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Cardiorespiratory Toxicity of Biomass Pollutants

Judith F. Ahounou Aïkpe , Jean-Bénoît M. Godonou, Maxim Senou, Credo R. Koukpoliyi, Armel Hounkonnou, Huguette B Akakpo, Joachim D. Gbenou, Pierre H. Dansou
American Journal of Medical Sciences and Medicine. 2021, 9(3), 70-74. DOI: 10.12691/ajmsm-9-3-2
Received May 27, 2021; Revised July 03, 2021; Accepted July 11, 2021

Abstract

Traditional biomass alone accounts for 8.5% of global energy consumption and exclusively covers the energy needs of nearly 3 billion people and 1.2 billion of whom do not yet have access to electricity. The smoke resulting from the combustion of this biomass contains various gases having harmful effects on health. This work aims to evaluate the toxic effects of carbon monoxide, methane and hydrogen sulfide on biochemical and cardiorespiratory parameters of Wistar rats. The complete blood count, C-reactive protein, lipid profile and histology of the lungs are evaluated after subchronic exposure to biomass smoke. The results showed a decrease in red blood cells (p = 0.004), an increase in blood platelets, an increase in C - reactive protein (p = 0.003) and triglycerides (p = 0.0041) and a decrease in HDL (p = 0, 0215) after 28 days of exposure. Exposure to smoke from biomass is therefore a source of alteration of cardiorespiratory parameters.

1. Introduction

Pollutants threaten the atmosphere, subsoil and oceans, as well as the species that live there 1. Their determination of their toxic effects is necessary for ecosystems’s protection. The specific health risks presented by these pollutants require a better understanding of their action mechanisms and call on various scientific disciplines. Recent and converging data from air pollution in literature suggest the presence of an effect of ambient air pollution on the risk of cardiorespiratory events 2.

During the latest estimates, published in World Health Organization 3 indicated that more than 7 million premature deaths in 2012 could be attributed to exposure to air pollution, including about 2 million 6 hundred thousand to pollution from outside. That is 1 in 8 deaths in the world. Majority of deaths from air pollution (51%) were mainly related to cardiovascular and respiratory diseases. Short-term links have been demonstrated between exposure to air pollution, particularly particulate matter, and the occurrence of ischemic heart disease. Other recent epidemiological studies have also noted a close relationship between recent exposure to particulate air pollution, especially pollution emitted by road traffic, and the occurrence of myocardial infarction 4, 5, 6, 7, 8.

However, in Benin as in other low-income countries, the high cost of gas and energy means that many households, both rural and urban, use wood for cooking food. These fuels and cooking methods produce high levels of air pollution in homes, which involves a multitude of pollutants harmful to health 7, 8, including fine particles that penetrate deep into the lungs and the blood. Several other studies have demonstrated the effect of biomass pollution on respiratory health 7, 9. Exposure to biomass smoke is responsible for respiratory worsening such as rhinitis, chronic bronchitis, obstructive ventilatory disorders and asthma symptoms 10.

This study aims to evaluate the toxic effects of carbon monoxide, methane and hydrogen sulfide on the lipid profile, inflammatory, biochemical, hematological parameters and pulmonary histology of animals.

2. Materials and methods

2.1. Ethics Statement

The Wistar rats used in this study were handled according to the Institutional animal safety guidelines (Animal facility, Faculty of Health Science, University of Abomey-Calavi, Benin). The experiments were performed according to the Institutional Animal Ethics No. 084 MS/DC/SG/DFRS/CNPERS/SA (University of Abomey Calavi, Benin).

2.2. Animal Specimen, Growth and Feeding Conditions

Ten weeks old Wistar rats (both male and female) with an average weight of 185,55 ± 6 g were kept in living conditions as recommended by the breeders (Sixty Wistar rats (60) aged 10-week-old male and female nulliparous Wistar strain with an average weight of 185.55 ± 6 and divided into 06 batches of 10 rats were used. They were supplied by the Research Unit in Effort Physiology of the National Institute of Youth, Physical Education and Sport (INJEPS).University of Abomey Calavi, Benin). The rats were kept in sets of six per

feeding device in standard wire mesh cages with stainless steel tray floor, in a room illuminated at 12 h light, 12 h dark at 25–30°C with relative humidity of 70-80 %. Rats were fed with diet composed of 53 % crushed maize, 19 % fish meal, 20 % wheat bran, 5 % groundnut oil, 1.5 % vitamin complex (Olivitasol), and 1.5 % NaCl. The chemical analysis of the diet was 16.1 % crude protein, 12.9 % crude fiber and 2.6 % crude fat. The diet and drinking water were provided ad libitum.

2.3. Gas Detection and Variation

The animals are divided into a control batch and a batch exposed to the fumes from biomass combustion under actual fish smoking conditions. Exposures are carried out for 28 day. The animals are placed in a closed cylindrical jar made of transparent glass for inhalation of the smoke from biomass. The closed cylindrical jar is connected to the fireplace used for the fish smoking activity by a pipe.

The concentration of gases inside cylindrical jar is taken before and after exposure of rats using a SENKO Portable Multi Gas Detector and Analyser. The gas analyser indicates on the screen the concentration of 4 gases (oxygen O2, carbon monoxide CO, hydrogen sulphide H2S, and methane CH4) simultaneously.

2.4. Determination of Blood Parameters

The sample is taken on the 7th, 14th, 28th and then on the 90th day after exposure according to guidelines 433 11 and 413 12 of the revised OECD standard, respectively. Blood parameters measured are white blood cells, red blood cells, hematocrit, hemoglobin, platelets and lymphocytes mean blood cell volume, mean blood cell hemoglobin concentration and mean blood cell hemoglobin content.

2.5. Determination of Biochemical Parameters

The determination of triglycerides, total cholesterol and HDL cholesterol are carried out in accordance with the prescriptions of the reagents of the kits of the Spanish group SPINREACT S.A.

2.6. Dissection

The animals are anesthetized by 0.5 ml of 2% lidocaine intraperitoneally. The abdominal cavity is incised, allowing observation of the abdominal viscera. The lungs are removed and opened with a scalpel blade for histological study.

2.7. Statistical Analysis

The statistical analyses of the results were carried out using Graph Pad prism Version 8.0.2 software. Comparisons of mean values were performed using parametric tests, including paired t-series tests after performing the Anova test on repeated measurements. The significance level is set at p ˂ 0.05.

3. Results

3.1. Cell Count, Hemoglobin Content and Hematocrit in Rats

The results of the blood count of the rats after exposure are compared with the results of the control rats (Table 1 and Table 2). Red blood cells dropped from the 7th day after exposure. The drop is significant in male rats on the 7th day (p = 0.022). In contrast, white blood cells increased significantly (p = 0.034) on the 7th day after exposure. Blood platelets or thrombocytes significantly increased on day 14 in both sexes. The increase was more significant in females (p = 0.0014).

3.2. C-Reactive-Protein (CRP)

The results show that CRP increased significantly from day 7 to day 28 after exposure (p= 0.003) in exposed animals before gradually falling on day 90 after exposure.

3.3. Lipid Profile

In both male and female rats, a significant increase (p = 0.0041) in triglycerides was observed from day 7. In contrast, HDL-cholesterol decreased from the 14th day after exposure (p = 0.0126) in male rats and (p = 0.0251) in female rats.

3.4. Histology of the Lungs

In control male or female rats, the lung parenchyma is typical with segmental bronchi (BS), pulmonary arteries (PA) and characteristic alveoli (A). After subchronic exposure, in both male and female rats, there is inflammatory infiltration which evolves into true lymphoid nodules (NL).

4. Discussion

Biochemical parameters are of primary importance in the assessment of many pathologies. They allow the evaluation of the possible toxic effect of an agent on the physiological functions of the organism 13. Environmental and physiological factors are known to affect many blood parameters. Hematological assessment in animals is of vital interest in the diagnosis of many diseases 14.

Analysis of the data in Tables I and II showed variation in blood parameters. There was a significant decrease (p = 0.022) in red blood cells associated with a significative increase (p = 0.034) in white blood cells and blood platelet count (p = 0.0014) in female rats. These changes are thought to be due to exposures to harmful pollutants from biomass burning smoke. Indeed, this smoke contains methane, hydrogen sulfide and a significant amount of carbon monoxide 15. The latter binds to hemoglobin to form carboxyhemoglobin (HbCO) which is not suitable for respiration. These results are similar to an Algerian study 16, 17. The significant drop in red blood cells associated with an increase in white blood cells from day 7 onwards is characteristic of an infection responsible for inflammation 18. This justifies the high level of trombocytes. Also, a significant increase (p = 0.003) in CRP was observed on day 14. Indeed, associations between many markers of inflammation and short and long term pollution exposure have been demonstrated 19. Exposure to biomass burning leads to airway inflammation and the effect is greater for high particle number concentrations 20. CRP increases very rapidly in response to infection and tissue damage. In addition, the indicators of chronic inflammation observed in the histological section of the lungs could justify the increase in CRP concentration. According to several studies, there is a strong correlation between increased environmental particulate matter and detrimental effects on pulmonary and cardiovascular health 21, 22. Pulmonary effects include increased frequency of asthma exacerbations and increased lung cancer deaths. Pulmonary inflammation caused by particulate matter could lead to a systemic increase in blood clotting 23, 24. The significant increase in triglycerides and the significant decrease in HDL levels have as direct consequences, the occurrence of complications related to hypercholesterolemia 25, 26, 27, 28. In fact, according to these authors, a high plasma concentration of very low density lipoprotein (VLDL) can explain at least in part a decrease in HDL-c in situations of metabolic syndrome.

Indeed, the increase of VLDL circulating stimulates in an exaggerated way the activity of the enzyme Cholesteryl ester transfer protein (CETP) which carries out exchanges of triglycerides and cholesterol between lipoproteins rich in triglycerides (VLDL, chylomicrons) and lipoproteins rich in (LDL, IDL, HDL).

This involved the increase of HDL with triglycerides and their depletion in cholesterol. In addition, the clearance of these HDL rich in triglyceride is increased.

These results are explained by the presence of the identified gases in the biomass smoke and are supported by a German study that showed that quitting smoking increases HDL cholesterol by about 10% 29. Other authors 30 have also justified that changes in HDL levels could occur even after brief exposure to air pollution.

5. Conclusion

Ultimately, air pollution is a major health problem. The results showed a variation of physiological parameters compared to controls. These variations would be responsible for the occurrence of cardio-respiratory diseases in women engaged in the activity of fish smoking.

References

[1]  Boukerche S., Aouacheri W., Saka S. Toxicological effects of nitrate: biological study in human and animal. Ann Biol Clin, 65 (4) : 385-91. 2007.
In article      
 
[2]  Zeller M., Royer C., Besancenot J.P., Cottin Y. Air pollution and cardiovascular disease. La Lettre du Cardiologue. (404): 14-9. 2007.
In article      
 
[3]  Who.int [Internet]. Pregny-Chambésy: Organisation Mondiale de la Santé. Aide-mémoire n°292.c1948-04 Février 2016; [Consulté le 22 Août 2016]. Disponible: http://ww.who.int/whr/2016/fr/index.html.
In article      
 
[4]  Peters A. Particulate matter and heart disease: Evidence from epidemiological studies. Toxicol Appl Pharmacol. 2005; 207(2 suppl): 477-82.
In article      View Article  PubMed
 
[5]  Lanki T., Pekkanen J., Aalto P. et al. Associations of traffi crelated air pollutants with hospitalisation for first acute myocardial infarction: the HEAPSS study. Occup Environ Med; 63(12): 844-51. 2006.
In article      View Article  PubMed
 
[6]  Zanobetti A., Schwartz J. Air pollution and emergency admissions in Boston, MA. J Epidemiol Community Health. 60: 890-5. 2006.
In article      View Article  PubMed
 
[7]  Kavouras I.G. et Chalbot M.C.G. Réponse inflammatoire, symptômes respiratoires et dégradation de la fonction respiratoire suite à l’exposition à la combustion de biomasse. Une perspective globale. Anses. Bulletin de veille scientifique. Santé / Environnement / Travail. (18): 23-6. 2012.
In article      
 
[8]  Ahounou Aïkpe F.J., Godonou M.J.B, Hounmondji E., Akakpo B.H., Gbenou D.J. and Dansou H.P. Effect of firewood smoking on the respiratory parameters of fish smokers. The Pharma Innovation Journal9(3): 697-702. 2020.
In article      View Article
 
[9]  Marano F., Aubier M., Brochard P., De Blay F., Marthan R., Nemery B., et al. Impact des particules atmosphériques sur la santé : aspects toxicologiques. Environnement, Risques et Santé. 3(2): 241-55. 2004.
In article      
 
[10]  Agodokpessi G., Ade G., Hinson V., Ade S., Okoumassou C.X., Fayomi B., et al. Prévalence des troubles respiratoires chez des femmes exerçant sur un site artisanal de fumage de poisson à Cotonou au Bénin. Mali Médical. Tome XXVI n°4: 34-8. 2011.
In article      
 
[11]  OECD (2018), Ligne directrice de l'ocde pour les essais de produits chimiques. Toxicité aiguë. Document 413. ENV Publications. Series on Testing and Assessment, Paris. 2018.
In article      
 
[12]  OECD (2018), Ligne directrice de l'ocde pour les essais de produits chimiques. Toxicité (subchronique) par inhalation: étude sur 90 jours. Document 413. ENV Publications. Series on Testing and Assessment, Paris. 2018.
In article      
 
[13]  Smaoui M., Ghurbel F., Buujelbene M., Makni-Ayadi F., El FEKI A. Impact de l'exposition chronique aux gaz d'échappement d'origine automobile sur certains biomarqueurs touchant la fonction hormonale sexuelle mâle, la fonction rénale et l'hémogramme chez le rat. Pollution Atmosphérique. (167): 439-49. 2000.
In article      View Article
 
[14]  Diaby V., Yapo A.F., Adon A.M., Yapi H.F., Djama A.J., Dosso M. 2016. Biotoxicité hématologique du sulfate de cadmium chez les rats Wistar. Int. J. Biol. Chem. Sci., 10(4): 1765-1772. 2016.
In article      View Article
 
[15]  Godonou J-B.M., Ahounou Aikpe J.F.., Koukpoliyi C. R., Hounkonnou A.., Akakpo H. B., Kotin L., Gbenou D. J., Dansou H. P. Toxicity of biomass pollutants in Wistar rats. IJMSIR- January - Vol – 6, Issue - 1, P. No. 235-241. 2021.
In article      
 
[16]  Tadjine A., Djebar H., Courtois A. Toxicité des poussières rejetées par le complexe sidérurgique d’Annaba sur quelques paramètres hématologiques du lapin Europeus. Environnement, Risques & Santé. 7 (3): 209-15. 2008.
In article      
 
[17]  Lefranc A., Larrieu S. Pollution atmosphérique et risque cardiovasculaire. Correspondances en Risque CardioVasculaire. 2008. 6 (1): 19-23.
In article      
 
[18]  Mathieu M., Guimezanes A. InflammatIon et maladies: clé de compréhension 2011-2012. 72p.
In article      
 
[19]  Ravindra K., Sokhi R., VanGrieken R. Atmospheric polyclyclic aromatic hydrocarbons: Source attribution, emission factors and regulation. Atmospheric Environment. 42: 2895-921. 2008.
In article      View Article
 
[20]  Rutter M.K., Meigs J.B., Sullivan L.M. et al. C-reactive protein, the metabolic syndrome, and prediction of cardiovascular events in the Framingham offspring study. Circulation. 110:380-5. 2004.
In article      View Article  PubMed
 
[21]  Pope III C.A., Burnett R.T., Thun M.J., et al. Lung cancer, cardiopulmonary mortality, and long-term exposure to fine particulate air pollution. JAMA. 287: 1132-41. 2002.
In article      View Article  PubMed
 
[22]  Delvin R.B., Ghio A.J., Kehrl H., Sanders G., Cascio W. Elderly humans exposed to concentrated air pollution particles have decreased heart rate variability. Eur Respir J. Suppl 40: 76-80. 2003.
In article      View Article  PubMed
 
[23]  Harrison R.M., Yin J. Particulate matter in the atmosphere: Which particle properties are important for its effects on health? Sci Total Environ 249: 85-101. 2000.
In article      View Article
 
[24]  Hajat S., Anderson H.R., Atkinson R.W., Haines A. Effects of air pollution on general practitioner consultations for upper respiratory diseases in London. Occup Environ Med. 59: 294-9. 2002.
In article      View Article  PubMed
 
[25]  Chagnon A. Contribution de certaines anomalies biologiques au diagnostic du paludisme. Med Mal Infect. 1999; 29 Suppl 3: 302-6.
In article      View Article
 
[26]  Montonen J., Boeing H., Fritsche A., Schleicher E., Joost H.G., Schulze M.B. et al. Consumption of red meat and whole-grain bread in relation to biomarkers of obesity, inflammation, glucose metabolism and oxidative stress. Eur J Nutr. 52(1): 337-45. Feb. 2013.
In article      View Article  PubMed
 
[27]  Sahach V.F., Korkach I.U.P., Kotsiuruba A.V., Prysiazhna O.D. The inhibition of oxidative and nitrosative stresses by ecdysterone as the mechanisms of its cardio- and vasoprotective action in experimental diabetes type I. Fiziol Zh. 54(5): 4654. 2008.
In article      
 
[28]  Boris Hansel, Alain Carrié, Éric Bruckert. Les hypo- et les hyper-HDLémies. Métabolismes Hormones Diabètes et Nutrition. XI (4): 167-74. 2007.
In article      
 
[29]  Walter F.R., Markus H. HDL bas-haut risque, HDL haut-faible risque ? 2008: 8(14): 24-62.
In article      View Article
 
[30]  Masson D., Yvan-Charvet L. L’augmentation du HDL-cholestérol Un traitement d’avenir dans le domaine de l’athérosclérose? Médecine/sciences 24: 341-74. 2008.
In article      View Article  PubMed
 

Published with license by Science and Education Publishing, Copyright © 2021 Judith F. Ahounou Aïkpe, Jean-Bénoît M. Godonou, Maxim Senou, Credo R. Koukpoliyi, Armel Hounkonnou, Huguette B Akakpo, Joachim D. Gbenou and Pierre H. Dansou

Creative CommonsThis work is licensed under a Creative Commons Attribution 4.0 International License. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/

Cite this article:

Normal Style
Judith F. Ahounou Aïkpe, Jean-Bénoît M. Godonou, Maxim Senou, Credo R. Koukpoliyi, Armel Hounkonnou, Huguette B Akakpo, Joachim D. Gbenou, Pierre H. Dansou. Cardiorespiratory Toxicity of Biomass Pollutants. American Journal of Medical Sciences and Medicine. Vol. 9, No. 3, 2021, pp 70-74. http://pubs.sciepub.com/ajmsm/9/3/2
MLA Style
Aïkpe, Judith F. Ahounou, et al. "Cardiorespiratory Toxicity of Biomass Pollutants." American Journal of Medical Sciences and Medicine 9.3 (2021): 70-74.
APA Style
Aïkpe, J. F. A. , Godonou, J. M. , Senou, M. , Koukpoliyi, C. R. , Hounkonnou, A. , Akakpo, H. B. , Gbenou, J. D. , & Dansou, P. H. (2021). Cardiorespiratory Toxicity of Biomass Pollutants. American Journal of Medical Sciences and Medicine, 9(3), 70-74.
Chicago Style
Aïkpe, Judith F. Ahounou, Jean-Bénoît M. Godonou, Maxim Senou, Credo R. Koukpoliyi, Armel Hounkonnou, Huguette B Akakpo, Joachim D. Gbenou, and Pierre H. Dansou. "Cardiorespiratory Toxicity of Biomass Pollutants." American Journal of Medical Sciences and Medicine 9, no. 3 (2021): 70-74.
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[1]  Boukerche S., Aouacheri W., Saka S. Toxicological effects of nitrate: biological study in human and animal. Ann Biol Clin, 65 (4) : 385-91. 2007.
In article      
 
[2]  Zeller M., Royer C., Besancenot J.P., Cottin Y. Air pollution and cardiovascular disease. La Lettre du Cardiologue. (404): 14-9. 2007.
In article      
 
[3]  Who.int [Internet]. Pregny-Chambésy: Organisation Mondiale de la Santé. Aide-mémoire n°292.c1948-04 Février 2016; [Consulté le 22 Août 2016]. Disponible: http://ww.who.int/whr/2016/fr/index.html.
In article      
 
[4]  Peters A. Particulate matter and heart disease: Evidence from epidemiological studies. Toxicol Appl Pharmacol. 2005; 207(2 suppl): 477-82.
In article      View Article  PubMed
 
[5]  Lanki T., Pekkanen J., Aalto P. et al. Associations of traffi crelated air pollutants with hospitalisation for first acute myocardial infarction: the HEAPSS study. Occup Environ Med; 63(12): 844-51. 2006.
In article      View Article  PubMed
 
[6]  Zanobetti A., Schwartz J. Air pollution and emergency admissions in Boston, MA. J Epidemiol Community Health. 60: 890-5. 2006.
In article      View Article  PubMed
 
[7]  Kavouras I.G. et Chalbot M.C.G. Réponse inflammatoire, symptômes respiratoires et dégradation de la fonction respiratoire suite à l’exposition à la combustion de biomasse. Une perspective globale. Anses. Bulletin de veille scientifique. Santé / Environnement / Travail. (18): 23-6. 2012.
In article      
 
[8]  Ahounou Aïkpe F.J., Godonou M.J.B, Hounmondji E., Akakpo B.H., Gbenou D.J. and Dansou H.P. Effect of firewood smoking on the respiratory parameters of fish smokers. The Pharma Innovation Journal9(3): 697-702. 2020.
In article      View Article
 
[9]  Marano F., Aubier M., Brochard P., De Blay F., Marthan R., Nemery B., et al. Impact des particules atmosphériques sur la santé : aspects toxicologiques. Environnement, Risques et Santé. 3(2): 241-55. 2004.
In article      
 
[10]  Agodokpessi G., Ade G., Hinson V., Ade S., Okoumassou C.X., Fayomi B., et al. Prévalence des troubles respiratoires chez des femmes exerçant sur un site artisanal de fumage de poisson à Cotonou au Bénin. Mali Médical. Tome XXVI n°4: 34-8. 2011.
In article      
 
[11]  OECD (2018), Ligne directrice de l'ocde pour les essais de produits chimiques. Toxicité aiguë. Document 413. ENV Publications. Series on Testing and Assessment, Paris. 2018.
In article      
 
[12]  OECD (2018), Ligne directrice de l'ocde pour les essais de produits chimiques. Toxicité (subchronique) par inhalation: étude sur 90 jours. Document 413. ENV Publications. Series on Testing and Assessment, Paris. 2018.
In article      
 
[13]  Smaoui M., Ghurbel F., Buujelbene M., Makni-Ayadi F., El FEKI A. Impact de l'exposition chronique aux gaz d'échappement d'origine automobile sur certains biomarqueurs touchant la fonction hormonale sexuelle mâle, la fonction rénale et l'hémogramme chez le rat. Pollution Atmosphérique. (167): 439-49. 2000.
In article      View Article
 
[14]  Diaby V., Yapo A.F., Adon A.M., Yapi H.F., Djama A.J., Dosso M. 2016. Biotoxicité hématologique du sulfate de cadmium chez les rats Wistar. Int. J. Biol. Chem. Sci., 10(4): 1765-1772. 2016.
In article      View Article
 
[15]  Godonou J-B.M., Ahounou Aikpe J.F.., Koukpoliyi C. R., Hounkonnou A.., Akakpo H. B., Kotin L., Gbenou D. J., Dansou H. P. Toxicity of biomass pollutants in Wistar rats. IJMSIR- January - Vol – 6, Issue - 1, P. No. 235-241. 2021.
In article      
 
[16]  Tadjine A., Djebar H., Courtois A. Toxicité des poussières rejetées par le complexe sidérurgique d’Annaba sur quelques paramètres hématologiques du lapin Europeus. Environnement, Risques & Santé. 7 (3): 209-15. 2008.
In article      
 
[17]  Lefranc A., Larrieu S. Pollution atmosphérique et risque cardiovasculaire. Correspondances en Risque CardioVasculaire. 2008. 6 (1): 19-23.
In article      
 
[18]  Mathieu M., Guimezanes A. InflammatIon et maladies: clé de compréhension 2011-2012. 72p.
In article      
 
[19]  Ravindra K., Sokhi R., VanGrieken R. Atmospheric polyclyclic aromatic hydrocarbons: Source attribution, emission factors and regulation. Atmospheric Environment. 42: 2895-921. 2008.
In article      View Article
 
[20]  Rutter M.K., Meigs J.B., Sullivan L.M. et al. C-reactive protein, the metabolic syndrome, and prediction of cardiovascular events in the Framingham offspring study. Circulation. 110:380-5. 2004.
In article      View Article  PubMed
 
[21]  Pope III C.A., Burnett R.T., Thun M.J., et al. Lung cancer, cardiopulmonary mortality, and long-term exposure to fine particulate air pollution. JAMA. 287: 1132-41. 2002.
In article      View Article  PubMed
 
[22]  Delvin R.B., Ghio A.J., Kehrl H., Sanders G., Cascio W. Elderly humans exposed to concentrated air pollution particles have decreased heart rate variability. Eur Respir J. Suppl 40: 76-80. 2003.
In article      View Article  PubMed
 
[23]  Harrison R.M., Yin J. Particulate matter in the atmosphere: Which particle properties are important for its effects on health? Sci Total Environ 249: 85-101. 2000.
In article      View Article
 
[24]  Hajat S., Anderson H.R., Atkinson R.W., Haines A. Effects of air pollution on general practitioner consultations for upper respiratory diseases in London. Occup Environ Med. 59: 294-9. 2002.
In article      View Article  PubMed
 
[25]  Chagnon A. Contribution de certaines anomalies biologiques au diagnostic du paludisme. Med Mal Infect. 1999; 29 Suppl 3: 302-6.
In article      View Article
 
[26]  Montonen J., Boeing H., Fritsche A., Schleicher E., Joost H.G., Schulze M.B. et al. Consumption of red meat and whole-grain bread in relation to biomarkers of obesity, inflammation, glucose metabolism and oxidative stress. Eur J Nutr. 52(1): 337-45. Feb. 2013.
In article      View Article  PubMed
 
[27]  Sahach V.F., Korkach I.U.P., Kotsiuruba A.V., Prysiazhna O.D. The inhibition of oxidative and nitrosative stresses by ecdysterone as the mechanisms of its cardio- and vasoprotective action in experimental diabetes type I. Fiziol Zh. 54(5): 4654. 2008.
In article      
 
[28]  Boris Hansel, Alain Carrié, Éric Bruckert. Les hypo- et les hyper-HDLémies. Métabolismes Hormones Diabètes et Nutrition. XI (4): 167-74. 2007.
In article      
 
[29]  Walter F.R., Markus H. HDL bas-haut risque, HDL haut-faible risque ? 2008: 8(14): 24-62.
In article      View Article
 
[30]  Masson D., Yvan-Charvet L. L’augmentation du HDL-cholestérol Un traitement d’avenir dans le domaine de l’athérosclérose? Médecine/sciences 24: 341-74. 2008.
In article      View Article  PubMed