Background: Particulate air pollution (PM) has been associated with increased mortality and morbidity from cardiovascular diseases but the mechanism linking PM inhalation with health effects is not completely understood. There is a growing burden of evidence that PM could produce alveolar and systemic inflammation and increase blood coagulation and risk of thrombosis. In a previous study we observed a shortened Prothrombin Time (PT) and no variation on Activated partial thromboplastin time (aPTT) in association with high ambient PM10 levels among healthy subjects in Milan, Italy. We investigated effects on blood clotting in a group of steel workers with well characterized exposure to high levels of PM. Methods: We enrolled 38 male workers employed in a steel production plant in Italy. Blood drawings in the first and in the last day of the working-week were obtained. Detailed individual information on occupational and medical history, smoking, life style and non-occupational exposure to PM were collected from either the existing plant medical records or personal interview. Measures of PM10, PM5 and PM1 were obtained during the working-week, using a GRIMM 1100 light-scattering dust analyzer, in 11 work areas of the steel production plant. Individual exposure was calculated as the average of PM concentration weighted by the time spent in each area by the subject. Mixed models were fitted to analyse the relation between PM exposure and coagulatory and inflammatory indexes, after adjustment for age, BMI, education, smoking and NSAIDs consumption. Results: Study subjects were exposed to PM levels 2–20 times higher than those to which general population is exposed (mean PM10 = 233 Kg/m3, range = 73–1220, mean PM1 = 8 Kg/m3, range = 2–30). We found elevated levels of inflammatory markers (intracellular adhesion molecules I-CAM and V-CAM) that further increased during the working week (P value for V-CAM = 0.002 and for I-CAM = 0.03). Average personal PM10 exposure was significantly associated with an increase of C-Reactive Protein levels ([beta] for 10 Kg/m3 of PM10 = +0.03, P = 0.01) and with shortened PT ([beta] = -0.02, P = 0.02). The same trend was confirmed considering PM5 and PM1 exposure. We observed no effects on aPTT. Conclusions: Our results show for the first time in an occupational setting that exposure to PM increases systemic inflammation and affect coagulation function, confirming the hypothesis that enhanced blood clotting may mediate air particle related cardiovascular effects in the general population.

PM exposure increases coagulation function : a study among highly exposed steel workers in Italy / M. Bonzini, A. Baccarelli, V. Pegoraro, L. Cantone, P. Grillo, P.A. Bertazzi, A. Tripodi, A. Artoni, P.M. Mannucci, P. Apostoli. - In: EPIDEMIOLOGY. - ISSN 1044-3983. - 19:6 suppl(2008 Nov), pp. S180-S180. ((Intervento presentato al 20. convegno ISEE : Annual Conference tenutosi a Pasadena, California nel 2008 [10.1097/01.ede.0000340048.78144.30].

PM exposure increases coagulation function : a study among highly exposed steel workers in Italy

M. Bonzini
Primo
;
A. Baccarelli
Secondo
;
L. Cantone;P. Grillo;P.A. Bertazzi;A. Tripodi;P.M. Mannucci
Penultimo
;
2008

Abstract

Background: Particulate air pollution (PM) has been associated with increased mortality and morbidity from cardiovascular diseases but the mechanism linking PM inhalation with health effects is not completely understood. There is a growing burden of evidence that PM could produce alveolar and systemic inflammation and increase blood coagulation and risk of thrombosis. In a previous study we observed a shortened Prothrombin Time (PT) and no variation on Activated partial thromboplastin time (aPTT) in association with high ambient PM10 levels among healthy subjects in Milan, Italy. We investigated effects on blood clotting in a group of steel workers with well characterized exposure to high levels of PM. Methods: We enrolled 38 male workers employed in a steel production plant in Italy. Blood drawings in the first and in the last day of the working-week were obtained. Detailed individual information on occupational and medical history, smoking, life style and non-occupational exposure to PM were collected from either the existing plant medical records or personal interview. Measures of PM10, PM5 and PM1 were obtained during the working-week, using a GRIMM 1100 light-scattering dust analyzer, in 11 work areas of the steel production plant. Individual exposure was calculated as the average of PM concentration weighted by the time spent in each area by the subject. Mixed models were fitted to analyse the relation between PM exposure and coagulatory and inflammatory indexes, after adjustment for age, BMI, education, smoking and NSAIDs consumption. Results: Study subjects were exposed to PM levels 2–20 times higher than those to which general population is exposed (mean PM10 = 233 Kg/m3, range = 73–1220, mean PM1 = 8 Kg/m3, range = 2–30). We found elevated levels of inflammatory markers (intracellular adhesion molecules I-CAM and V-CAM) that further increased during the working week (P value for V-CAM = 0.002 and for I-CAM = 0.03). Average personal PM10 exposure was significantly associated with an increase of C-Reactive Protein levels ([beta] for 10 Kg/m3 of PM10 = +0.03, P = 0.01) and with shortened PT ([beta] = -0.02, P = 0.02). The same trend was confirmed considering PM5 and PM1 exposure. We observed no effects on aPTT. Conclusions: Our results show for the first time in an occupational setting that exposure to PM increases systemic inflammation and affect coagulation function, confirming the hypothesis that enhanced blood clotting may mediate air particle related cardiovascular effects in the general population.
Settore MED/09 - Medicina Interna
Settore BIO/12 - Biochimica Clinica e Biologia Molecolare Clinica
Settore MED/44 - Medicina del Lavoro
nov-2008
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Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/2434/54794
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