Giulia Cesaroni

Ms. Giulia Cesaroni

orcid

Research Focus & Metrics

Academic Career Length

31Years (1996-Present)

(Calculated once Scilit publication data is synced: current year − year of first publication + 1)

Representative Publications

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4 September 2018 in Proceedings of the National Academy of Sciences
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RBRichard Burnett
Richard Burnett
HCHong Chen
Hong Chen
MSMieczyslaw Szyszkowicz
Mieczyslaw Szyszkowicz
NFNeal Fann
Neal Fann
BHBryan Hubbell
Bryan Hubbell
JSJoseph V. Spadaro
Joseph V. Spadaro
Exposure to ambient fine particulate matter (PM2.5) is a major global health concern. Quantitative estimates of attributable mortality are based on disease-specific hazard ratio models that incorporate risk information from multiple PM2.5sources (outdoor and indoor air pollution from use of solid fuels and secondhand and active smoking), requiring assumptions about equivalent exposure and toxicity. We relax these contentious assumptions by constructing a PM2.5-mortality hazard ratio function based only on cohort studies of outdoor air pollution that covers the global exposure range. We modeled the shape of the association between PM2.5and nonaccidental mortality using data from 41 cohorts from 16 countries—the Global Exposure Mortality Model (GEMM). We then constructed GEMMs for five specific causes of death examined by the global burden of disease (GBD). The GEMM predicts 8.9 million [95% confidence interval (CI): 7.5–10.3] deaths in 2015, a figure 30% larger than that predicted by the sum of deaths among the five specific causes (6.9; 95% CI: 4.9–8.5) and 120% larger than the risk function used in the GBD (4.0; 95% CI: 3.3–4.8). Differences between the GEMM and GBD risk functions are larger for a 20% reduction in concentrations, with the GEMM predicting 220% higher excess deaths. These results suggest that PM2.5exposure may be related to additional causes of death than the five considered by the GBD and that incorporation of risk information from other, nonoutdoor, particle sources leads to underestimation of disease burden, especially at higher concentrations.

1 August 2013 in The Lancet Oncology
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Journal Article
Closed access
OROle Raaschou-Nielsen
Ole Raaschou-Nielsen
ZAZorana J Andersen
Zorana J Andersen
RBRob Beelen
Rob Beelen
ESEvangelia Samoli
Evangelia Samoli
Massimo StafoggiaMassimo Stafoggia
Massimo Stafoggia
GHGerard Hoek
Gerard Hoek

1 March 2014 in The Lancet
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Journal Article
Closed access
RBRob Beelen
Rob Beelen
OROle Raaschou-Nielsen
Ole Raaschou-Nielsen
Massimo StafoggiaMassimo Stafoggia
Massimo Stafoggia
ZAZorana Jovanovic Andersen
Zorana Jovanovic Andersen
GWGudrun Weinmayr
Gudrun Weinmayr
GHGerard Hoek
Gerard Hoek

1 October 2012 in Environmental Science & Technology
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Journal Article
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Marloes EeftensMarloes Eeftens
Marloes Eeftens
RBRob Beelen
Rob Beelen
KHKees de Hoogh
Kees de Hoogh
TBTom Bellander
Tom Bellander
GCGiulia Cesaroni
Giulia Cesaroni
GHGerard Hoek
Gerard Hoek

1 June 2013 in Atmospheric Environment
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Journal Article
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RBRob Beelen
Rob Beelen
GHGerard Hoek
Gerard Hoek
DVDanielle Vienneau
Danielle Vienneau
Marloes EeftensMarloes Eeftens
Marloes Eeftens
KDKonstantina Dimakopoulou
Konstantina Dimakopoulou
KHKees de Hoogh
Kees de Hoogh

21 January 2013 in BMJ
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Journal Article
Open access
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GCGiulia Cesaroni
Giulia Cesaroni
FFFrancesco Forastiere
Francesco Forastiere
Massimo StafoggiaMassimo Stafoggia
Massimo Stafoggia
ZAZorana J Andersen
Zorana J Andersen
CBCHIARA BADALONI
CHIARA BADALONI
APAnnette Peters
Annette Peters
Objectives To study the effect of long term exposure to airborne pollutants on the incidence of acute coronary events in 11 cohorts participating in the European Study of Cohorts for Air Pollution Effects (ESCAPE). Design Prospective cohort studies and meta-analysis of the results. Setting Cohorts in Finland, Sweden, Denmark, Germany, and Italy. Participants 100 166 people were enrolled from 1997 to 2007 and followed for an average of 11.5 years. Participants were free from previous coronary events at baseline. Main outcome measures Modelled concentrations of particulate matter <2.5 μm (PM2.5), 2.5-10 μm (PMcoarse), and <10 μm (PM10) in aerodynamic diameter, soot (PM2.5 absorbance), nitrogen oxides, and traffic exposure at the home address based on measurements of air pollution conducted in 2008-12. Cohort specific hazard ratios for incidence of acute coronary events (myocardial infarction and unstable angina) per fixed increments of the pollutants with adjustment for sociodemographic and lifestyle risk factors, and pooled random effects meta-analytic hazard ratios. Results 5157 participants experienced incident events. A 5 μg/m3 increase in estimated annual mean PM2.5 was associated with a 13% increased risk of coronary events (hazard ratio 1.13, 95% confidence interval 0.98 to 1.30), and a 10 μg/m3 increase in estimated annual mean PM10 was associated with a 12% increased risk of coronary events (1.12, 1.01 to 1.25) with no evidence of heterogeneity between cohorts. Positive associations were detected below the current annual European limit value of 25 μg/m3 for PM2.5 (1.18, 1.01 to 1.39, for 5 μg/m3 increase in PM2.5) and below 40 μg/m3 for PM10 (1.12, 1.00 to 1.27, for 10 μg/m3 increase in PM10). Positive but non-significant associations were found with other pollutants. Conclusions Long term exposure to particulate matter is associated with incidence of coronary events, and this association persists at levels of exposure below the current European limit values.