European Journal of Internal Medicine 57 (2018) 49–57

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European Journal of Internal Medicine

journal homepage: www.elsevier.com/locate/ejim

Original Article

Mortality and morbidity for cardiopulmonary diseases attributed to PM2.5 T

exposure in the metropolis of Rome, Italy
⁎
Alessandra De Marcoa, Patrick Amoateyb, Yusef Omidi Khaniabadic, Pierre Sicardd, ,
Philip K. Hopkee,f
a
Italian National Agency for New Technologies, Energy and Sustainable Economic Development, Rome, Italy
b
Department of Biology, Sultan Qaboos University, Al-Khould, Muscat, Oman
c
Health Care System of Karoon, Ahvaz Jundishapur University of Medical Sciences, Ahvaz, Iran
d
ARGANS, Sophia Antipolis, France
e
Center for Air Resources Engineering and Science, Clarkson University, Potsdam, USA
f
Department of Public Health Sciences, University of Rochester School of Medicine and Dentistry, Rochester, USA

A R T I C LE I N FO A B S T R A C T

Keywords: The aim of the study was to evaluate the health effects associated with the exposure to ground-level of parti-
AirQ+ model culate matters with aerodynamic diameter ≤ 2.5 μm (PM2.5) on citizens in Rome (Italy) in 2015 and 2016. Based
Hospital admissions on the new version of the World Health Organization's AirQ+ model, we have estimated the short- and long-
Mortality term effects of PM2.5 on hospital admissions due to cardiovascular (HA-CVD) and respiratory diseases (HA-RD)
Relative risk
as well as on mortality for ischemic heart disease (M-IHD) and chronic obstructive pulmonary disease (M-COPD).
Rome
In this study, city-specific relative risk values and baseline incidence rates were used to calculate the association
PM2.5
between PM2.5 and daily counts of emergency hospitalizations and mortality. The annual mean PM2.5 con-
centrations were 18 μg m−3 and 14 μg m−3 in 2015 and 2016, respectively. In Rome, the citizens are mostly
exposed to daily mean PM2.5 concentrations of 10–20 μg m−3 during the study period. In 2015–2016, 0.4–0.6%
for HA-CVD, 1.1–1.5% for HA-RD, 16.5–18.1% for M-IHD and 8.5–9.2% for M-COPD are attributed to PM2.5. In
2015–2016, 134–186 HA-CVD, 126–175 HA-RD, 947–1037 M-IHD and 244–279 M-COPD, caused by PM2.5 ex-
posure, could be “avoided” if PM2.5 concentrations would not exceed 10 μg m−3, i.e. the threshold recommended
by the World Health Organization. Thus, a consistent air quality management and sustainable city planning are
needed, urgently, to mitigate the adverse effects of PM2.5 exposure in Rome.

1. Introduction
Global population in urban cities are expected to rise 60% by 2060
[5]. In a typical urban environment, citizens are exposed to about 200
air pollutants (e.g. SO2, O3, NO2 and PM10) or classes of air pollutants
[33, 70] and their concentrations vary with time and location [40, 41].
Air pollution is a major environmental issue in urban areas affecting
quality of life and citizens' well-being [24]. Therefore, air pollution
across the most populated cities around the globe is a major concern to
policy-makers [37, 38, 50, 53]. In cities, tropospheric ozone and par-
ticulate matter with an aerodynamic diameter of 2.5 μm (PM2.5) are the
most threatening air pollutants [4, 23, 28, 33, 45]. Urban population of
the European Union (EU) exceeding EU reference levels for human
health protection was in the range of 9–14% for PM2.5 [23, 78].
The PM2.5 are emitted from both natural (e.g. pollen, mineral dust)
and anthropogenic sources (e.g. road traffic) where local meteor-
ological conditions are important factor determining their concentra-
tion levels [1, 4, 46, 59, 69, 72]. Previous studies showed that PM2.5 is
strongly associated with mortality and morbidity due to respiratory and
cardiovascular diseases [9, 20, 30, 33, 40, 41, 43, 47]. The available
information does not allow a judgment to be made of concentrations
below which no effects would be expected [78]. Despite the air quality
standards implementation since the early 1990s, with significant re-
ductions in emissions of common air pollutants, epidemiological studies
show that ambient particulate matter including PM2.5 could cause
about 3.1 million deaths per year [46] and about 479,000 deaths in
Europe [78].
Most respiratory diseases (RD) occur as a result of deposition and
penetration of PM2.5 on the walls of respiratory tracts [9, 12]. Metal
bound PM2.5 such as nickel and copper could reduce the efficacy of

⁎
Corresponding author.
E-mail address: psicard@argans.eu (P. Sicard).

https://doi.org/10.1016/j.ejim.2018.07.027
Received 9 June 2018; Received in revised form 29 July 2018; Accepted 31 July 2018
Available online 16 August 2018
0953-6205/ © 2018 Published by Elsevier B.V. on behalf of European Federation of Internal Medicine.
A. De Marco et al.
endothelial linings of the cardiovascular system to cause cardiovascular
diseases (CVD) [57]. A short-term exposure to ambient PM2.5 can cause
ischemic heart diseases (IHD) and chronic obstructive pulmonary
(COPD) deaths [35, 48]. The COPD is irreparable blockage of airways
caused by inflammatory of the lungs due to deposition of PM2.5 [6].
Epidemiological studies indicated a significant correlation between
ambient PM2.5 exposure and the incidence of COPD [39]. A meta-
analysis reported that exposure to ambient PM2.5 exceeding 10 μg m−3
could increase the risk of COPD mortality by 2.5% [44]. At global scale,
the ambient PM2.5 exposure caused about 1,078,800 and 242,250
deaths due to IHD and COPD, respectively, in 2012 [78].
In Rome (Italy), high PM2.5 concentrations occur during summer,
exceeding the EU target value (i.e. 25 μg m−3 as annual mean) for
human health protection [61]. The PM2.5 emissions are one of the
biggest health concerns in Rome [51, 62, 64] and come mostly from
biomass combustions, road traffic, geogenic sources, coastal areas and/
or long-range transport of dust from desert areas, e.g. Saharan dust [8,
26]. Avino et al. [9] investigated the effect of PM2.5, from dense traffic
roads in Rome, and showed that during traffic peak hours, about
6.6 × 1010 particles are deposited into the respiratory system of citizens
in proximity of traffic.
A report of the Committee on the Medical Effects of Air Pollutants
stresses on PM2.5 as the air pollutant most strongly associated with
increased mortality and morbidity risks [19]. In European cities, a
10 μg.m−3 increase in PM2.5 generates an increase in daily hospital
admissions [70], e.g. for respiratory diseases (+0.28%) and chronic
obstructive pulmonary diseases (+0.4%) and an increase in daily
mortality, e.g. for cardiovascular (+0.5%) and respiratory (+1.1%)
causes. Extensive research has demonstrated the associations between
short- and long-term PM2.5 exposure and ill-health endpoints of re-
spiratory and cardiovascular diseases and daily mortality as observed in
epidemiological, clinical and toxicological studies over the past two
decades in Italy (e.g. [2, 7, 11, 17, 63, 65, 66, 73, 83]). The associations
between fine particles and daily mortality and morbidity were high-
lighted by the results from large epidemiological studies through the
MED-PARTICLES project [65, 73] or from a cohort of more than a
million adults in Rome [17].
Quantifying hospital admissions has been feasible due to air quality
health risk assessment impact model (AirQ) developed by the WHO's
regional office for Europe [53]. This model has been widely used and
applied in several studies in most cities in the world (e.g. [12, 40, 41,
54, 56, 60]). The AirQ model allows users to perform health risk as-
sessment of wide range of air pollutants obtained, either from air
quality monitoring stations or from air dispersion modeling systems
[14]. For a given air pollutant and health outcome, other input para-
meters, such as baseline incidence rate and number of exposed popu-
lation, are required [40, 41].
Due to limited knowledge on PM2.5 effects on hospital admissions
and mortality in Rome, the main objective of this study is to evaluate
the hospital admissions due to respiratory and cardiovascular diseases
(including stroke) attributed to short-term PM2.5 exposure, as well as
the long-term effects of PM2.5 on IHD and COPD mortality by using the
new AirQ+ modeling system in 2015 and 2016. The new findings have
an important role in establishing the World Health Organization
Guidelines and in implementing EU-target values and regional-level
policies aimed at reducing emissions and concentrations of PM2.5.
2. Materials and methods
2.1. Study location
The study was conducted in Rome located 20 km inland with a total
area of 1285 km2 (Fig. 1). The population in Rome was estimated at
2,864,731 inhabitants in 2015 and at 2,873,494 inhabitants in 2016.
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European Journal of Internal Medicine 57 (2018) 49–57
The Italian capital is characterized by four distinct climates including
winter (−5 °C), spring (18 °C), summer (35 °C) and autumn (23 °C). In
summer, the Rome metropolis experiences warm-wind from south-
eastern part of the country carrying suspended fine particulate matter
from sub-Sahara Africa [61]. The mean annual precipitation is
837.3 mm during the study period. The densely populated city of Rome
has heavy traffic road (mostly cars, buses and trucks) of about 3 million
vehicles (about 40% of diesel-fueled engine vehicles) where the vehicle
to resident ratio is estimated to be 706:1000 for a total area of
1287 km2 [9].
2.2. Evaluation of the health impact
For the health risk assessment of air pollution, the software AirQ+
(v1.0) is an updated version of the previous model AirQ2.2.3 [3, 12, 31,
40, 41]. The AirQ+ model was developed by the WHO Regional Office
for Europe and it is a valuable tool used to estimate the mortality and
morbidity due to exposure to ambient air pollutants. Similar to the
previous version, AirQ+ employs epidemiological data including re-
lative risk (RR) values, attribute proportion (AP) and baseline incidence
rate (BI) together with in-situ air pollution data (from monitoring sta-
tion or modeling) of an exposed population data to simulate the short-
and long-term health effects of a given city [10, 31, 56, 79].
For a health endpoint, the RR values, associated with an increase of
10 μg m−3 of the air pollutant concentration, are obtained from the
published exposure-response relative risk functions [70] and measure
the probability of developing a disease relative to exposure (Eq. 1).
RR = exp.[β(X − X 0)] (1)
where β is a parameter that regulates the rate of RR increment, X
(μg m−3) is the measured air pollutant concentration and X0 (μg m−3) is
the background concentration where no health effect is reported [4]. A
relative risk of 1 indicates there is no increase in risk. The Health Im-
pact Assessment results are presented as per 10 μg m−3 increase in
PM2.5 levels.
In the AirQ+ software, the quantification of mortality due to adult
COPD and IHD due to long-term exposure to PM2.5 is based on in-
tegrated exposure-response functions from European cohort studies
[15, 36, 76].
⎧ if z ≥ z cf then RR(z) = 1 + α {1–exp[−γ (z − z cf )δ]}
⎨ if z < z cf then RR(z) = 1 (2)
⎩
−3
where z is the annual PM2.5 concentration (in μg m ) and zcf is the
counterfactual PM2.5 concentration below which we assumed there is
no additional risk. The coefficient α, γ and δ are pre-integrated AirQ+
parameters [15].
The attribute proportion (AP) is the fraction of health endpoint due
to air pollutant exposure on a given population [12, 32, 50, 55]. The AP
is calculated by using the RR values for a specific health endpoint and
air pollutant “c” (i.e. PM2.5). P(c) is the proportion of the population
exposed to PM2.5 (Eq. 3):
AP = ∑ { [ RR(c) − 1] × P(c ) } ÷ ∑ {RR(c) × P(c ) } (3)
The rate of health outcome attributable to the PM2.5 exposure (IE) is
calculated as (Eq. 4):
IE = BI × AP (4)
where IE is the rate of the health impact attributable to the PM2.5 ex-
posure and BI is the baseline incidence (per 100,000 inhabitants) of the
considered health endpoints in an exposed group [14, 79].
Knowing the number of exposed inhabitants (N) in a city and IE
from Eq. (4), the number of excess cases (NE) attributable to the PM2.5
exposure is calculated as (Eq. 5):
A. De Marco et al. European Journal of Internal Medicine 57 (2018) 49–57

Fig. 1. Locations of air quality monitoring stations in Rome metropolis - Agenzia Regionale per la Protezione dell'Ambiente del Lazio.

Table 1 Table 2
Baseline incidence (per 100,000 inhabitants) and relative risk with 95% con- Annual averages and standard deviations of hourly PM2.5 concentrations (in μg
fidence intervals (CI) per 10 μg m−3 increase in PM2.5 for daily hospital ad- m−3) at 9 urban stations where PM2.5 are measured in Rome in 2015 and 2016.
missions due to cardiovascular diseases (HA-CVD) and respiratory diseases (HA-
Station Typology Average ± SD (μg. m−3)
RD) and mortality for ischemic heart diseases (M-IHD) and chronic obstructive
pulmonary diseases (M-COPD) due to long-term PM2.5 exposure in Rome [17, 2015 2016
27, 73].
1- Villa Ada Background urban 16.1 ± 10.2 14.7 ± 9.0
Health effect Baseline incidence Relative Risk per 10 μg m−3 (95% CI)
2- Francia Traffic 20.6 ± 10.2 17.2 ± 9.0
7- Arenula Background urban 16.9 ± 9.6 14.8 ± 10.3
HA-CVD 1130 1.0051 (1.0012–1.0090)
8- Cipro Background urban 17.5 ± 10.9 14.4 ± 9.3
HA-RD 400 1.0136 (1.0023–1.0249)
10- Guido Background urban 14.7 ± 8.0 12.5 ± 12.2
M-IHD 199 Integrated exposure-response functions
11- Cinecitta Background urban 21.8 ± 15.9 17.5 ± 11.2
M-COPD 106
12- Cavaliere Background urban 18.1 ± 11.2 15.6 ± 9.7
13- Malagrotta Background suburban 17.1 ± 12.1 18.5 ± 17.6
14- Guidonia Background suburban 18.0 ± 11.0 14.6 ± 9.8
NE = IE × N (5) Rome metropolis 17.9 ± 7.3 14.4 ± 11.4

In this study, city-specific RR and baseline incidence rates were used

(Table 1) and are based on local information provided by published
epidemiological studies and by the MED-PARTICLES project which
calculated the short-term association between PM2.5 and mortality and
daily counts of emergency hospitalizations for cardiovascular and re-
spiratory diseases in Rome over the time period 2001–2010 [65, 73].
An increase of 10 μg m−3 in PM2.5 was associated with increases in
cardiovascular admissions (including stroke) of 0.51% (95% CI:
0.12–0.90%) and respiratory hospitalizations: 1.36% (95% CI:
0.23–2.49). Faustini et al. [27] analyzed a population-based cohort (≥
35 years of age) living in Lazio region in the period 1998–2000 and
found a BI value of 106 per 100,000 inhabitants for mortality for
chronic obstructive pulmonary diseases (M-COPD). Cesaroni et al. [17]
reported a BI rate of 199 for mortality for ischemic heart diseases (M-
IHD).
2.3. Exposure assessment of PM2.5
Air pollution data were provided by the Environmental Department
of the Municipality of Rome (EDMR). This agency is responsible for
collection, storage and dissemination of PM2.5 from the monitoring
stations located within the city of Rome. The real-time air quality
monitoring stations measure several air pollutants including PM2.5. The
24-hourly PM2.5 data were collected from 9 monitoring sites, from 1st
January to 31st December in 2015 and 2016, across Rome metropolis
(Fig. 1). Urban background monitoring sites were given priority to
better represent average exposure. The data from one station “traffic”
and two stations “suburban” were included to have a larger spatial
representativeness (Table 2). Only monitors with at least 75% of vali-
dated hourly data per month were considered eligible. The city-specific
daily mean of PM2.5 concentrations was derived for each station by
averaging hourly values from the available monitors.
3. Results
3.1. Temporal variations PM2.5
The lowest annual mean PM2.5 concentrations recorded is
14.7 μg m−3 and 12.5 μg m−3 in 2015 and 2016 respectively (Guido
station, far from city center) and the highest annual mean PM2.5 con-
centrations (21.8 μg m−3 in 2015) was observed at Cinecitta station
along a main road (Table 2). By joining all data from all stations, we
observe that the annual mean of PM2.5 (Table 2) was higher in 2015
(17.9 μg m−3) compared to 2016 (14.4 μg m−3) while the maximum
annual 24-h mean was higher in 2016 (99.0 μg m−3) than 2015
(82.0 μg m−3). All stations exceed the limit values established by the
WHO (10 μg m−3) for human health protection in Europe (Fig. 2).
Fig. 3 presents seasonal mean PM2.5 concentrations for the four
seasons (winter, spring, summer and fall) in Rome city. The fall season
showed higher PM2.5 concentrations with 21.9 μg m−3 and 18.9 μg m−3
in 2015 and 2016, respectively, and the lowest PM2.5 concentrations are
recorded in summer (14.0 μg m−3 in 2015 and 11.4 μg m−3 in 2016).
People living in Rome were mainly exposed to PM2.5 concentrations,
ranging from 10 to 20 μg m−3 from 1st January 2015 to 31st December
2016 (Fig. 4). The PM2.5 concentrations were lower than 18 μg m−3
(15 μg m−3) for half of the year 2015 (2016) and 72% (83%) of the year
were below a daily PM2.5 concentration of 25 μg m−3.
3.2. Adverse health effect of PM2.5 on population
Table 3 presents the estimated AP (%) and the number of cases of
HA-CVD, HA-RD, M-IHD and M-COPD due to short- and long-term
PM2.5 exposure based on published city-specific BI and RR values and
integrated exposure-response functions (Table 1).

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A. De Marco et al. European Journal of Internal Medicine 57 (2018) 49–57

Fig. 2. Annual mean PM2.5 concentrations in each station in Rome in 2015 and 2016. The red lines represent the limit values established by the WHO (10 μg m−3)
and European Commission (25 μg m−3) for health protection in Europe. (For interpretation of the references to colour in this figure legend, the reader is referred to
the web version of this article.)

The attributed proportion of HA-CVD and HA-RD due to short-term
PM2.5 exposure is 0.58% and 1.53% in 2015 and 0.41% and 1.10% in
2016, respectively. In 2015, the AirQ+ results indicate that 186 HA-
CVD and 175 HA-RD, caused by short-term exposure to PM2.5, could be
“avoided” if PM2.5 concentrations would not exceed 10 μg m−3, which
happens to be the threshold recommendation by the WHO Air Quality
Guidelines (2006). The number of excess cases was 134 for HA-CVD
and 126 for HA-RD in 2016 (Table 3). In 2015, the number of HA-CVD
could lead to 6.5 × 105 cases, while HA-RD could affect 6.1 × 105
people in Rome when PM2.5 concentrations are beyond 10 μg m−3.
The M-IHD attributed to PM2.5 exposure is high, i.e. 18.1% in 2015
and 16.5% in 2016 (Table 3). If PM2.5 concentrations do not exceed
10 μg m−3, around 900–1000 premature deaths for IHD caused by long-
term PM2.5 exposure could be “avoided” each year. The number of
excess cases for COPD mortality is 279 in 2015 and 244 in 2016. In
2015, the number of cases for IHD could lead to 36.2 × 105 deaths,
while deaths for COPD could affect 9.7 × 105 people in Rome city when
PM2.5 concentrations are beyond 10 μg m−3. The 95% confident in-
terval represents the uncertainty values associated with AirQ+ model
estimation.
In 2015 and 2016, the highest number of morbidity is related to the
PM2.5 concentrations range 17–24 μg m−3 producing significant health
impacts on the inhabitants of Rome (Fig. 5). For both HA-CVD and HA-RD,
50% (90%) of the health impacts of the residents occurred in days with
PM2.5 concentrations are lower than 28 μg m−3 (32 μg m−3) and
23 μg m−3 (47 μg m−3) in 2015 and 2016, respectively (data not shown).

Fig. 3. Seasonal mean PM2.5 concentrations (in μg m−3) in Rome in 2015 and 2016 over the period January–March (JFM), April–June (AMJ), July–September (JAS)
and October–December (OND).

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A. De Marco et al. European Journal of Internal Medicine 57 (2018) 49–57

Fig. 4. Number of days per different concentrations of PM2.5.

Table 3 average PM2.5 concentration is of 19.6 μg m−3 over the time period
AirQ+ estimated attributed proportion (AP, in %), estimated attributable cases 2006–2010 [2] while Cesaroni et al. [17] have registered a mean PM2.5
(number of cases) and estimated of attributable cases per 100,000 population at exposure of 23 μg m−3 between 2001 and 2010. The PM2.5 mean value
risk for short-term PM2.5 exposure for daily hospital admissions due to cardi- (24 μg m−3) recorded by Marconi et al. [51] in Rome, in April 2001
ovascular diseases (HA-CVD) and respiratory diseases (HA-RD) and mortality through March 2003, is higher compared to our results. These previous
for ischemic heart diseases (M-IHD) and chronic obstructive pulmonary dis-
studies show that the PM2.5 levels are widely variable over space and
eases (M-COPD) due to long-term PM2.5 exposure in Rome, with lower and
time.
upper limits of the relative risk 95% confident interval (95% CI).
Temporal daily counts of emergency hospitalizations for cardio-
Year Health Estimated AP (%) Excess cases Attributable cases per vascular diseases (HA-CVD) and respiratory diseases (HA-RD) as well as
effect 100,000 people
the mortality due to COPD and IHD were evaluated from short- and
2015 HA-CVD 0.58 (0.14–1.01) 186 (44–328) 6.50 (1.53–11.44) long-term PM2.5 exposures for two successive years (2015–2016) in
HA-RD 1.53 (0.26–2.77) 175 (30–318) 6.10 (1.04–11.09) Rome.
M-IHD 18.10 1037 36.20 (24.72–47.57) In the framework of the MED-PARTICLES project, by using a meta-
(12.36–23.78) (708–1363)
smoothing approach and city-specific Poisson models, significant as-
M-COPD 9.18 (3.85–16.04) 279 (117–487) 9.73 (4.08–17.00)
2016 HA-CVD 0.41 (0.10–0.73) 134 (32–237) 4.67 (1.10–8.23) sociations were found between PM2.5 and HA-RD and HA-CVD
HA-RD 1.10 (0.19–2.00) 126 (21−230) 4.40 (0.75–8.01) (Stafoggia et al., 2010; [65]). An increase of 10 μg m−3 in PM2.5 was
M-IHD 16.48 947 32.95 (22.58–43.08) associated with increases in cardiovascular admissions of 0.51% (95%
(11.29–21.54) (649–1238) CI: 0.12–0.90%) and of 1.36% (95% CI: 0.23–2.49) for respiratory
M-COPD 8.03 (2.91–13.59) 244 (87–406) 8.51 (3.09–14.40)
hospitalizations (Stafoggia et al., 2010). From these RR values, i.e.
RR = 1.0051 for HA-CVD and RR = 1.0136 for HA-RD, the AirQ+
4. Discussions results indicate that, 186 HA-CVD and 175 HA-RD could be “avoided” if
PM2.5 concentrations would not exceed 10 μg m−3 in 2015, i.e. the
The newly developed AirQ+ software is a valuable health risk as- threshold recommendation by the WHO Air Quality Guidelines (2006).
sessment modeling system used to evaluate the short- and long-term Belleudi et al. [11] reported that 9275 hospital admissions for RD
health impacts of outdoor air pollution affecting human health world- were due to PM2.5 inhalation in Rome over the time period 2001–2005
wide (e.g. [31]; Khaniabadi et al., 2017; [50]; WHO, 2018; [76]). (annual mean PM2.5: 23 μg m−3). The excess risk for HA-RD was esti-
Guerreiro et al. [34] analyzed data for all EU-member states from 2002 mated to be 2.8% (95% CI: 0.5–5.2%) per 10 μg/m3 increase in PM2.5.
to 2011 and found that air pollutants in PM2.5 decreased substantially To reduce uncertainties of epidemiological data at city scale, Bravo
in all areas. In Italy, the total PM2.5 emissions decreased by 24% over et al. [13] investigated relationships between HA-RD and HA-CVD with
the time period 2001–2012. The PM2.5 concentrations for 2015–2016 short-term PM2.5 exposure for 708 counties in United States (U·S) for 48
are higher in fall (19–22 μg m−3) compared to summer (11–14 μg m−3) million Medicare beneficiaries. The results revealed that an increase of
due to higher road traffic emissions, industrial activities and long-range 0.35% in HA-CVD (95% CI: -0.71-1.41%) and of 2.57% in HA-RD (95%
transport of wind-blown particles during cold period [8, 11]. CI: 0.90–4.30%) is observed per 10 μg m−3 increase in PM2.5 [13].
In this study, the recorded annual mean PM2.5 concentrations are, Dominici et al. [22] similarly reported that for 204 urbanized counties
on average, of about 18 μg m−3 in 2015 and 14 μg m−3 in 2016 over the in U.S, with > 200,000 inhabitants, a 10 μg m−3 increase in ambient
study area. These annual means exceed the air quality standards fixed PM2.5 could increase the risk of HA-CVD by 1.28% (95% CI:
by the WHO (10 μg/m3) and respect the EU-target value (25 μg m−3). 0.78–1.78%). In Istanbul, an excess risk of 1.50% (95%: 1.09–1.99%)
From January 2016 to January 2017, Fanizza et al. [26] have reported for HA-RD was found over the time period 2013–2015, especially for
a similar annual mean (16 μg m−3) for PM2.5 concentrations, de- children and elderly population, i.e. vulnerable people [16]. In Beijing,
termined by gravimetric analysis, in Rome. In Rome, the annual with 20 million people, during days with high 24-h PM2.5 levels

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A. De Marco et al.
Fig. 5. Relationship between number of excess cases for HA-CVD (a), HA-RD (b) and PM2.5 concentration intervals in 2015 and 2016 in Rome metropolis.
(exceeding of 100 μg m−3), the excess risk of HA-CVD and HA-RD are
53% (95% CI: 29–82) and 38% (95% CI: 5–76), respectively for
10 μg m−3 increment in PM2.5 levels [75].
Cesaroni et al. [17] analyzed a population-based cohort, 1,265,058
people ≥30 years-old living in Rome, over the time period 2001–2010,
using Cox regression models to estimate associations with cause-specific
mortality for different individual groups (e.g. sex, age, residential his-
tory, marital status, occupation) and area characteristics. From October
2001 to December 2010, 151,807 deaths were registered including 15%
for IHD (i.e. BI = 199 per 100,000 inhabitants), 9% for cerebrovascular
diseases, and 6% for respiratory diseases. A cohort of 26,039 patients
(35+ years old) of the Lazio region in Italy hospitalized with a COPD
was enrolled in the period 1998–2000 [27], the BI rate for M-COPD was
106 per 100,000 inhabitants (95% CI: 0.98–1.13). Base on published
integrated exposure-response functions [15] and BI rates [17, 27], we
found that the number of excess cases for IHD and COPD mortality is
1037 and 279 in 2015 and 947 and 244 in 2016, respectively.
A 10 μg m−3 increase in PM2.5 was associated with an increase in
54
European Journal of Internal Medicine 57 (2018) 49–57
IHD of 1.10% (95% CI: 1.06–1.13%), 1.01% increase (95% CI:
0.99–1.05%) in respiratory mortality and 1.04% increase (95% CI:
1.03–1.05) in CVD mortality [17]. By applying a RR = 1.0110 for M-
IHD rather than integrated exposure-response functions as proposed by
the AirQ+ software, the number of excess cases for M-IHD is strongly
lower, i.e. 71 in 2015 and 51 in 2016. Similarly, by applying a
RR = 1.0029 (0.9962–1.0096) for M-COPD [15], the number of excess
cases is lower, i.e. 10 in 2015 and 7 in 2016.
A meta-analysis over 12 Mediterranean cities (including Rome)
were performed over the time period 2001–2010 and showed that an
increase in PM2.5 was associated with 1.11% (95% CI: 0.19–2.04%)
increase in cardiovascular mortality and 2.49% (95% CI: 0.92–4.07%)
increase in respiratory mortality [65]. Alessandrini et al. [2] selected
228,619 natural deaths of elderly persons (≥65 year-old) in 12 Italian
cities during the time period 2006–2010. The percentage change as-
sociated with a 10 μg m−3 increase in PM2.5 were 1.30% (95% CI: -0.16-
2.78) in natural mortality, 1.44% (95% CI: 0.07–2.82) in IHD, 1.47%
(95% CI: -0.55-3.53) in CVD and 1.07% (95% CI: -0.27-2.44) in COPD.
A. De Marco et al.
Michelozzi et al. [52] examined the relationship between PM2.5 ex-
posure with mortality in metropolitan area of Rome over the study
period 1992–1995 and reported an increase of 0.29% (95% CI: -0.90-
1.47%) in respiratory mortality and of 0.37% (−0.07–0.82%) in car-
diovascular mortality per 10 μg m−3 increment.
Hadei et al. [35] estimated the M-IHD in Iranian megacity of Tehran
due to long-term exposure PM2.5 with higher annual mean concentra-
tions of 40 and 38 μg m−3 in 2014 and 2015, respectively. The number
of cases per 100,000 people for M-IHD was 86 and [84] in Tehran for
2014 and 2015, respectively [35] while in Rome the number of cases
are around 36 per 100,000 people in 2015. Cohen et al. [18] applied
11 km × 11 km resolution satellite imagery and integrated Exposure-
Response functions to estimated global burden of disease from ambient
PM2.5 exposure, results showed that ambient global PM2.5 levels in-
creased over a 25-year time period and the PM2.5 and caused 1521.1
IHD (95% CI: 1231.7–1821.2) and 863.6 COPD (95% CI: 538.5–1212.8)
deaths for a 10 μg m−3 increase in PM2.5 concentrations. In Taiwan, a
study reported that PM2.5 exposure caused 2244 deaths (95% CI:
2015–2473) and 645 deaths (95% CI: 418–872) for IHD and COPD,
respectively in 2014 due to PM2.5 [48]. Similarly, long-term PM2.5 ex-
posure contributes to 171 pre-matured IHD deaths and 77 pre-matured
COPD deaths in 161 cities in China in 2015 [49]. In greater Cairo
(Egypt), the AP for M-IHD could reach 30% (95% CI: 21–48%) and 23%
(95% CI: 21–32%) for M-COPD with an annual mean PM2.5 con-
centration of 75 μg m−3 [76] while in Rome the AP is of 16.5% for M-
IHD and 9.2% for M-COPD in 2015. According to Song et al. [71], in
China where about 1.3 billion residents are at health risk from PM2.5
exposure, 30.2% of deaths (IHD, COPD, stroke and lung cancer) are
attributable to ambient PM2.5 from 1st January 2014 to 31st December
2016. In Beijing, time-series investigation conducted in 2010–2012
showed that a 10 μg m−3 increase in PM2.5 levels causes an increase of
0.25% (95% CI: 0.10–0.40%) in M-IHD [82]. An increase of 10 μg m−3
in PM2.5 is known associated with an increase of 1.05% (95% CI:
1.02–1.08%) in M-IHD among 445,860 adults in 100 U.S cities [74].
5. Conclusion
Information on the short- and long-term effects of PM2.5 on mor-
bidity in Southern Europe will be useful to inform European policies on
air quality standards. The current version of AirQ+ model offers an
opportunity to evaluate health effects of ambient air pollutant affecting
human health. This model was used to model short- and long-term ef-
fects of hospital admissions due to CVD and RD as well as mortality for
COPD and IHD due to PM2.5 exposure of residents in Rome in
2015–2016. We observed that the current PM2.5 concentration levels in
Rome exceed (1.5 times on average) the annual threshold limits set by
the WHO while the levels are in agreement with EU-target values in
2015 and 2016. Particulate matters are threatening air pollutants and is
becoming a major environmental issue in Rome affecting quality of life
and citizens' well-being [80, 81].
The Health Impact Assessment is applied exactly when the evidence
from epidemiology is enough to support a causal association and the
best estimate (RR and BI) indicating the association is applied in spe-
cific locations taking into account local exposure levels and baseline
rates. Modeled outputs based on city-specific BI and RR values, reveals
that in 2015, 186 HA-CVD and 175 HA-RD in addition to 1037 M-IHD
and 279 M-COPD caused by PM2.5 exposure could be “avoided” if PM2.5
concentrations would not exceed 10 μg m−3, which happens to be the
threshold recommendation by the WHO Air Quality Guidelines (2006).
This study provides crucial information in curbing current and fu-
ture morbidity and mortality problems from ambient particulate matter
short-term exposures. The study is focused on PM2.5 only, it would be
necessary to assess the health impacts of other air pollutants (e.g.
ozone). In cities, the ozone background level is rising due to a lower
ozone titration by NO due to the reduction in local NOx emissions [68].
Such increases would exceed target values for the protection of human
55
European Journal of Internal Medicine 57 (2018) 49–57
health, crops and forests. In cities, the rising ground-level ozone pol-
lution appears as a major air quality issue in urban areas and becomes a
public health concern affecting trees, biodiversity and well-being of
citizens [67].
To overcome these sanitary problems, it will be beneficial in ex-
ploring alternative preventive measures of safeguarding human health
from air pollution through policy actions and air quality management
programs. For instance, previous studies have provided quantitative
estimates of the ability of urban vegetation to ameliorate urban air
quality (e.g. particulate matter) across conurbations worldwide (e.g.
[58]). The vegetation intercepts particulate matter on plant surfaces,
absorbs gaseous pollutants through the leaf stomata and can affect the
transport of polluted air masses, e.g. by reducing ventilation of street
canyons. To reduce ground-level PM in cities, it is important to define
efficient city planning. For that, municipalities need to clearly under-
stand the magnitude of urban vegetation effects on air pollution.
Even PM2.5 for this study may consist of several heavy metals and
ions where the study could not assessed their individual health impacts
due to hospital admission as they lead to synergic effects. The model
being ecological other than epidemiological function may not account
for behavioral differences among the exposed population. In addition,
there are several days of missing data; this may affect the actual PM2.5
value and modeled results. Also, the two-year PM2.5 data may not be
adequate to better predict their contribution to human health effects.
Air dispersion modeling of the PM2.5 data might have assumed uniform
distribution and dilution of the pollutants taking into consideration,
impact of meteorological factors (temperature, wind, pressure, and
precipitation) to the pollutants concentration to which the Rome city
residents may be exposed.
Acknowledgement
The authors wish to thank the Environmental Department of the
Municipality of Rome for providing the PM2.5 emission data and the
Ahvaz Jundishapur University of Medical Sciences for supporting
(ETRC-9636).
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