RATIONALE Acute and chronic exposure to particulate air pollution has been associated with increased risk of cardiovascular and respiratory disease. Processes related to cardiorespiratory outcomes, such as oxidative stress, atherosclerosis, aging have been associated with lower global DNA methylation content in blood DNA. Whether DNA methylation is modified by air particle exposure has never been tested. METHODS We estimated global DNA methylation through analysis of LINE1 and Alu repeated elements in 1,006 blood DNA samples from the Normative Aging Study (NAS), a repeated measure investigation of elderly men in Boston. DNA methylation was measured analysis of bisulfite-treated blood DNA by PCR-Pyrosequencing. We used mixed models to estimate the effects of ambient level of particle number (PN), black carbon (BC), and particulate matter<2.5 m (PM2.5) on DNA methylation RESULTS LINE1 DNA methylation was decreased after recent exposure (3-5 day moving averages) to higher PM or BC concentrations. The strongest association was observed with the 4-day average for PN (=-0.123, 95%CI -0.186, -0.059; p=0.004) and the 5-day average for BC (=-0.082; 95%CI -0.145, -0.019; p=0.01). Non significant decreases were found in Alu repeated sequences. PM2.5 showed only non-significant associations with LINE1 and Alu methylation. CONCLUSIONS Short-term exposure to particles, particularly those from traffic sources, may decrease DNA methylation. These findings suggest a novel biological mechanism that may reproduce aging processes and potentially mediate the effects of particulate air pollution on human health.

Effects of short-term exposure to particulate air pollution on blood DNA methylation / A. Baccarelli, R.O. Wright, V. Bollati, L. Tarantini, A. Litonjua, H. Suh, D. Sparrow, P. Vokonas, J. Schwartz. ((Intervento presentato al convegno American Thoraric Society 2008 tenutosi a Toronto nel 2008.

Effects of short-term exposure to particulate air pollution on blood DNA methylation

A. Baccarelli
Primo
;
V. Bollati;L. Tarantini;
2008

Abstract

RATIONALE Acute and chronic exposure to particulate air pollution has been associated with increased risk of cardiovascular and respiratory disease. Processes related to cardiorespiratory outcomes, such as oxidative stress, atherosclerosis, aging have been associated with lower global DNA methylation content in blood DNA. Whether DNA methylation is modified by air particle exposure has never been tested. METHODS We estimated global DNA methylation through analysis of LINE1 and Alu repeated elements in 1,006 blood DNA samples from the Normative Aging Study (NAS), a repeated measure investigation of elderly men in Boston. DNA methylation was measured analysis of bisulfite-treated blood DNA by PCR-Pyrosequencing. We used mixed models to estimate the effects of ambient level of particle number (PN), black carbon (BC), and particulate matter<2.5 m (PM2.5) on DNA methylation RESULTS LINE1 DNA methylation was decreased after recent exposure (3-5 day moving averages) to higher PM or BC concentrations. The strongest association was observed with the 4-day average for PN (=-0.123, 95%CI -0.186, -0.059; p=0.004) and the 5-day average for BC (=-0.082; 95%CI -0.145, -0.019; p=0.01). Non significant decreases were found in Alu repeated sequences. PM2.5 showed only non-significant associations with LINE1 and Alu methylation. CONCLUSIONS Short-term exposure to particles, particularly those from traffic sources, may decrease DNA methylation. These findings suggest a novel biological mechanism that may reproduce aging processes and potentially mediate the effects of particulate air pollution on human health.
mag-2008
Settore MED/44 - Medicina del Lavoro
http://www.abstracts2view.com/ats08/
Effects of short-term exposure to particulate air pollution on blood DNA methylation / A. Baccarelli, R.O. Wright, V. Bollati, L. Tarantini, A. Litonjua, H. Suh, D. Sparrow, P. Vokonas, J. Schwartz. ((Intervento presentato al convegno American Thoraric Society 2008 tenutosi a Toronto nel 2008.
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Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/2434/59571
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