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Cardiovascular disease burden from ambient air pollution in Europe reassessed using novel hazard ratio functions

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Aims: Ambient air pollution is a major health risk, leading to respiratory and cardiovascular mortality. A recent Global Exposure Mortality Model, based on an unmatched number of cohort studies in many countries, provides new hazard ratio functions, calling for re-evaluation of the disease burden. Accordingly, we estimated excess cardiovascular mortality attributed to air pollution in Europe. Methods and results: The new hazard ratio functions have been combined with ambient air pollution exposure data to estimate the impacts in Europe and the 28 countries of the European Union (EU-28). The annual excess mortality rate from ambient air pollution in Europe is 790 000 [95% confidence interval (95% CI) 645 000-934 000], and 659 000 (95% CI 537 000-775 000) in the EU-28. Between 40% and 80% are due to cardiovascular events, which dominate health outcomes. The upper limit includes events attributed to other non-communicable diseases, which are currently not specified. These estimates exceed recent analyses, such as the Global Burden of Disease for 2015, by more than a factor of two. We estimate that air pollution reduces the mean life expectancy in Europe by about 2.2 years with an annual, attributable per capita mortality rate in Europe of 133/100 000 per year. Conclusion: We provide new data based on novel hazard ratio functions suggesting that the health impacts attributable to ambient air pollution in Europe are substantially higher than previously assumed, though subject to considerable uncertainty. Our results imply that replacing fossil fuels by clean, renewable energy sources could substantially reduce the loss of life expectancy from air pollution.
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Cardiovascular disease burden from ambient air
pollution in Europe reassessed using novel
hazard ratio functions
Jos Lelieveld
1,2
*, Klaus Klingmu¨ ller
1
,Andrea Pozzer
1
,Ulrich Po¨ schl
1
,
Mohammed Fnais
3
,Andreas Daiber
4,5
, and Thomas Mu¨nzel
4,5
*
1
Max Planck Institute for Chemistry, Hahn-Meitner-Weg 1, 55128 Mainz, Germany;
2
The Cyprus Institute, 20 Kavafi Street, 2123 Nicosia, Cyprus;
3
King Saud University, College
of Science, Riyadh 11451, Saudi Arabia;
4
Center for Cardiology, Cardiology I, Angiology and Intensive Care Medicine, University Medical Center of the Johannes Gutenberg
University, Langenbeckstrasse 1, 55131 Mainz, Germany; and
5
German Center for Cardiovascular Research (DZHK), Partner Site Rhine-Main, Langenbeckstr. 1, 55131 Mainz,
Germany
Received 18 November 2018; revised 5 December 2018; editorial decision 22 February 2019; accepted 22 February 2019; online publish-ahead-of-print 12 March 2019
See page 1597 for the editorial comment on this article (doi: 10.1093/eurheartj/ehz200)
Aims Ambient air pollution is a major health risk, leading to respiratory and cardiovascular mortality. A recent Global
Exposure Mortality Model, based on an unmatched number of cohort studies in many countries, provides new haz-
ard ratio functions, calling for re-evaluation of the disease burden. Accordingly, we estimated excess cardiovascular
mortality attributed to air pollution in Europe.
........................................................................ ............. ............. ............. .................. ............. ............. .................. ......................
Methods
and results
The new hazard ratio functions have been combined with ambient air pollution exposure data to estimate the
impacts in Europe and the 28 countries of the European Union (EU-28). The annual excess mortality rate from am-
bient air pollution in Europe is 790 000 [95% confidence interval (95% CI) 645 000–934 000], and 659 000 (95%
CI 537 000–775 000) in the EU-28. Between 40% and 80% are due to cardiovascular events, which dominate
health outcomes. The upper limit includes events attributed to other non-communicable diseases, which are cur-
rently not specified. These estimates exceed recent analyses, such as the Global Burden of Disease for 2015, by
more than a factor of two. We estimate that air pollution reduces the mean life expectancy in Europe by about
2.2 years with an annual, attributable per capita mortality rate in Europe of 133/100 000 per year.
........................................................................ ............. ............. ............. .................. ............. ............. .................. ......................
Conclusion We provide new data based on novel hazard ratio functions suggesting that the health impacts attributable to am-
bient air pollution in Europe are substantially higher than previously assumed, though subject to considerable un-
certainty. Our results imply that replacing fossil fuels by clean, renewable energy sources could substantially reduce
the loss of life expectancy from air pollution.
䊏䊏䊏䊏䊏䊏䊏䊏䊏䊏䊏䊏䊏䊏䊏䊏䊏䊏䊏䊏䊏䊏䊏䊏䊏䊏䊏䊏䊏䊏䊏䊏䊏䊏䊏䊏䊏䊏䊏䊏䊏䊏䊏䊏䊏䊏䊏䊏䊏䊏䊏䊏䊏䊏䊏䊏䊏䊏䊏䊏䊏䊏䊏䊏䊏䊏䊏䊏䊏䊏䊏䊏䊏䊏䊏䊏䊏䊏䊏䊏䊏䊏䊏䊏䊏䊏䊏䊏䊏䊏䊏䊏䊏䊏䊏䊏䊏䊏䊏䊏䊏䊏䊏䊏䊏䊏䊏䊏䊏䊏䊏䊏䊏䊏䊏䊏䊏䊏䊏䊏䊏䊏䊏䊏䊏䊏䊏䊏䊏䊏䊏䊏䊏䊏䊏䊏䊏䊏䊏䊏䊏䊏䊏䊏䊏䊏䊏䊏䊏䊏䊏䊏䊏䊏䊏䊏䊏䊏䊏䊏䊏䊏䊏䊏䊏䊏䊏䊏䊏䊏䊏䊏䊏䊏䊏䊏䊏䊏䊏䊏䊏䊏䊏䊏䊏䊏䊏䊏䊏䊏䊏䊏䊏䊏䊏䊏䊏䊏䊏䊏䊏䊏䊏䊏䊏䊏䊏䊏䊏䊏䊏䊏
Keywords Air pollution Fine particulate matter Excess mortality rate Loss of life expectancy Cardiovascular
risk Health promotion intervention
Introduction
According to the World Health Organization (WHO), non-
communicable diseases (NCD) are the globally leading cause of mor-
tality.
1
About 71% of 56 million deaths that occurred worldwide in
2015 are attributed to NCD, mainly cardiovascular diseases (CVD,
31%), cancers, diabetes, and chronic lung diseases. In Europe, CVD
account for 45% of the mortality rate, and within the 28 countries of
the European Union (EU-28) it is 37%.
1,2
This amounts to 2.14 million
and 1.85 million deaths per year, respectively.
1
Well-known risk
* Corresponding author. Tel: þ49 6131 305 4000, Fax: þ49 6131 305 4019, Email: jos.lelieveld@mpic.de; Tel: þ49 6131 17 7250, Fax: þ49 6131 17 6615,
Email: tmuenzel@uni-mainz.de
V
CThe Author(s) 2019. Published by Oxford University Press on behalf of the European Society of Cardiology.
This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/4.0/),
which permits non-commercial re-use, distribution, and reproduction in any medium, provided the original work is properly cited. For commercial re-use, please contact
journals.permissions@oup.com
European Heart Journal (2019) 40, 1590–1596 CLINICAL RESEARCH
doi:10.1093/eurheartj/ehz135 Prevention and epidemiology
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factors include tobacco smoking, unhealthy diets, lack of physical ac-
tivity, overweight, raised blood pressure, blood sugar, and choles-
terol, which can be either avoided or substantially reduced. It is
estimated that 80% of premature heart disease, stroke, and diabetes
can be prevented.
1
Environmental factors, in particular air pollution,
pose additional risks with health implications that have been underes-
timated in the Global Burden of Disease (GBD).
3
Chronic exposure
to enhanced levels of fine particle matter impairs vascular function,
which can lead to myocardial infarction, arterial hypertension, stroke,
and heart failure.
4,5
Predominant sources of fine particulates are fossil
fuel and biomass combustion, industry, agriculture, and wind-blown
dust.
6
While air pollution is often ignored as a health risk factor,
2
the
Lancet Commission on pollution and health recommends air quality ac-
tion plans for the prevention and control of NCD.
3
The commission
estimated that about nine million excess deaths worldwide are attrib-
utable to degraded environmental conditions, of which about half to
ambient (outdoor) air pollution, being the main environmental health
risk. Previously we estimated that the excess mortality rate from air
pollution, related to CVD, amounts to 2.4 million per year, of which
269 000 in Europe.
7
These estimates combine exposure of the popu-
lation to fine ambient particulates with disease-specific hazard ratios
from epidemiological cohort studies.
8
The underlying biomedical and
chemical mechanisms are not fully resolved, but there is mounting
evidence of a causal relationship between the exposure to fine
particulate matter with a diameter below 2.5 mm(PM
2.5
)andcardio-
vascular morbidity and mortality.
3,912
Mechanistic factors include
PM
2.5
-induced inflammation, oxidative stress, and vascular (endothe-
lial) dysfunction, which can facilitate the development of hyperten-
sion, diabetes, and atherosclerosis, with a possibly much larger health
impact than expected.
11
To update the estimates of CVD mortality attributable to PM
2.5
,
we applied recent hazard ratio functions in a new Global Exposure
Mortality Model (GEMM), based on a large number of cohort stud-
ies,
13
employing a much extended database and range of exposures
than the recent GBD assessment for 2015.
8,14
The new hazard func-
tions complement those of the GBD for 2015, including new infor-
mation on NCDs.
13
Five disease categories, i.e. lower respiratory
tract illness (LRI), chronic obstructive pulmonary disease (COPD),
lung cancer (LC), ischaemic heart disease (IHD), and cerebrovascular
disease (CEV) leading to stroke, have been identified, similar to ear-
lier assessments.
8,14
The new GEMM also identifies a category non-
accidental diseases, defined as NCD þLRI, and by subtracting the
above categories, we derive one that is referred to as ‘other NCD’.
Here, we show that air pollution is a much larger mortality factor
than previously assumed, especially from CVD, associated with a
mean loss of life expectancy (LLE) of more than two years in Europe.
We discuss the mechanistic factors that may explain the large impact
of air pollution on CVD.
Methods
Model calculated exposure
The global exposure of the population to air pollution in the year 2015
has been computed through data-informed modelling (for details, see
Supplementary material online). We used the EMAC atmospheric
chemistry–climate model, which comprehensively simulates atmospheric
chemical and meteorological processes and interactions with the land,
oceans, and biosphere.
15,16
The model computes exposure by accounting
for the atmospheric chemistry of natural and anthropogenic emissions,
leading to PM
2.5
and gaseous oxidants such as ozone (O
3
).
6,7
The EMAC
model development is pursued by an international consortium (https://
www.messy-interface.org). This website offers additional model descrip-
tion, references, and model output. The software is publicly available
through a community end-user license agreement. The model is continu-
ally evaluated through comparison to measurement data from ground-
based networks, field campaigns, and satellite remote sensing. We applied
the model configuration described by Lelieveld et al.
7
Emission categories
were defined according to Lelieveld et al.,
6
updated for the year 2015,
with fossil sources from power generation, industry and traffic, and add-
itional anthropogenic sources from residential energy use (biofuels), agri-
culture, and biomass burning.
7
Global Exposure Mortality Model
While we applied the same model calculations of air pollution, baseline
mortality and population data of the WHO for the year 2015 used previ-
ously,
7
we revised our results by using the new hazard ratio functions
given by the GEMM of Burnett et al.,
13
which is based on 41 cohort stud-
ies in 16 countries. These functions relate hazard ratios to air pollution
concentrations, being dependent on age and geographical location (usual-
ly country level). Applying them to model calculated pollution concentra-
tions, in combination with population data and baseline mortality rates of
the WHO,
1
yields excess mortality rates in the five defined disease cate-
gories (LRI, COPD, IHD, CEV, and LC), plus the difference between
NCD þLRI and the former five, yielding the ‘other NCD’. While the lat-
ter cannot be specified, below we argue that it is significantly associated
with CVD mortality.
The GEMM accounts for a much larger range of air pollution concen-
trations than the GBD of 2015, by including new cohort data from China,
where air quality tends to be poorer than in Europe and North America
from where epidemiological data have dominated former GBD assess-
ments.8,14 Figure 1illustrates the consequences of using the expanded
database in the GEMM, and the large differences in hazard ratios com-
pared with the GBD 2015. For additional examples, we refer to
Supplementary material online, Figure S1 of Burnett et al.
13
While for
GBD 2015 the available PM
2.5
observations extended from a few mg/m
3
to about 35 mg/m
3
, the new data include much higher concentrations up
to 84 mg/m
3
, encompassing 97% of all relevant cases.
13
The limited infor-
mation at high PM
2.5
concentrations was hitherto made up for by using
data from second-hand and active smoking studies, which apparently lead
to an underestimate of hazard ratios, for example by allowing the number
of IHD and CEV events to increase only marginally at high PM
2.5
concentrations.
8
Results
Burden of disease
Previously we estimated a global mortality rate attributable to ambi-
ent air pollution by PM
2.5
and O
3
of 4.55 [95% confidence interval
(95% CI) 3.41–5.56] million in 2015,
7
in close agreement with the
GBD 2015.
8,14
The 95% CIs express uncertainty in epidemiological
data.
8,13
With the new GEMM we estimate 8.79 (95% CI 7.11–10.41)
million in 2015. This agrees well with the global estimate of 8.9 (95%
CI 7.5–10.3) of Burnett et al.
13
To put this into perspective, the
WHO estimates that the excess death rate from tobacco smoking is
CVD burden from ambient air pollution in Europe 1591
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7.2 million per year
17
; hence air pollution is now rated as the larger
risk factor. The new GEMM leads to a doubling of the air pollution at-
tributable mortality. It corresponds to a global mean per capita mor-
tality rate of 120/year per 100 000 inhabitants. In Europe, the per
capita rate exceeds the global mean with 133/year per 100 000, and
129/year per 100 000 in the EU-28 (Table 1). We find that especially
in eastern Europe per capita mortality rates are very high, for ex-
ample in Bulgaria, Croatia, Romania, and the Ukraine, where they ex-
ceed 200/year per 100 000. Table 1also presents the years of life lost
(YLL) and the LLE. In Europe, the number of YLL is 14 (95% CI 12–
17) million/year, and the mean LLE is 2.2 (95% CI 1.8–2.6) years. The
LLE in Europe from air pollution attributable CVD alone is 1.0 (95%
CI 0.9–1.2) year, and 1.8 (95% CI 1.2–2.5) years if we also include the
other NCD.
Large health impact through
cardiovascular disease
Table 1and Supplementary material online, Table S1 list disease cate-
gories that contribute to excess mortality from air pollution. It
presents results for Europe, the EU-28, and the five countries that
are leading in terms of total CVD mortality as well as attributable
CVD deaths. Cerebrovascular events in Europe contribute 64 000
(95% CI 31 000–95 000) per year. This includes ischaemic and haem-
orrhagic strokes, with about 38 000 and 26 000 per year, respective-
ly. The attributable IHD mortality rate in Europe is 313 000 (95% CI
286 000–339 000) per year. Note that the uncertainty range for CEV
is larger than for IHD, which is illustrated by the 95% CIs in Figure 1.
Supplementary material online, Table S1 provides disease-itemized
and country-level results, including the minimum and maximum val-
ues defined by the CIs.
Figure 2presents a map of attributable CVD mortality, showing
relatively high incidence in the south-eastern UK, the Benelux,
Germany, northern Italy, and eastern European countries. The total
excess CVD mortality rate in Europe is 377 000 (95% CI 317 000
434 000) per year, and in the EU-28 it is 264 000 (95% CI 221 000
304 000) per year. This represents 48% and 40%, respectively, of the
total excess mortality rate related to all disease categories. Figure 3
shows the allocation to different diseases in the EU-28, which cor-
roborates the major role of CVD mortality. It also emphasizes the
significant increase between the GBD 2015 and the new estimates,
especially for IHD events. The total mortality rate from air pollution
in the EU-28 has more than doubled with the new GEMM, from
about 263 000 to 659 000 per year. To a large extent this is explained
by the category ‘other NCD’, previously not accounted for.
The WHO states that CVD make the relatively largest contribu-
tion to NCD deaths (by 41%), followed by cancers, respiratory dis-
eases, and diabetes. Since the categories LRI, COPD, and LC,
included in the GEMM, account for the known respiratory and LC
events, it appears that at least part of the mortality rate from air pol-
lution by other NCD, being 1.74 (95% CI 0.96–3.29) million/year glo-
bally, must be credited to CVD events, which encompass a wide
range of diseases. We find that in Europe other NCD contribute
255 000 (95% CI 115 000–394 000) per year to excess mortality, and
in the EU-28 it is 249 000 (95% CI 132 000–365 000) per year. The
total attributable CVD mortality rate in the EU-28 of 1.85 million/
year is made up by 633 000 from IHD (34%), 426 000 from CEV
(stroke) (23%) and 790 000 per year by other CVD (43%).
2
In view
of this considerable fraction of ‘other CVD’ we hypothesize that a
PM (µg/m )
2.5 3
GBD 2015
GEMM
PM (µg/m )
2.5 3
GBD 2015
GEMM
AB
Figure 1 Hazard ratios as a function of annual mean PM
2.5
, referring to cerebrovascular disease (A) and ischaemic heart disease (B) (after ref.
13
).
Solid lines show the range for which epidemiological data are available, and the dashed ones extrapolate to higher concentrations. For Global Burden
of Disease 2015, the extrapolation was based on smoking studies. Shaded areas show 95% confidence intervals. CEV, cerebrovascular disease; GBD,
Global Burden of Disease; GEMM, Global Exposure Mortality Model; IHD, ischaemic heart disease; PM
2.5
, fine particulate matter with a diameter
below 2.5 mm.
1592 J. Lelieveld et al.
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large fraction of the air pollution related mortality from other NCD
coincides with other CVD.
Air pollutants such as PM
2.5
, as well as the gaseous compounds O
3
and nitrogen dioxide (NO
2
), may aggravate atherosclerosis through
yet non-explicitly identified risk factors that cause CVD mortality,
which may include diabetes and hypertension. Below we argue that
general pathways of health impacts by particulate and gaseous pollu-
tants impair vascular function, which may explain their remarkably
large influence on excess mortality rates through the combined IHD,
CEV, and other NCD events. In the upper limit, i.e. by assuming that
all other NCD deaths occur through cardiovascular events, the
mortality rate from air pollution by CVD in Europe would account
for about 80% of the total (and about 78% within the EU-28).
Discussion
Air pollution mortality in Europe
The relatively high attributable per capita mortality rate in Europe of
about 133/year (and 129/year in the EU-28) per 100 000 is explained
by the combination of poor air quality and dense population, leading
to exposure that is among the highest in the world. We reiterate that
.........................................................................................................................................................
....................................................................................................................................................................................................................
Table 1 Estimated annual excess mortality attributed to air pollution
a
All risks From air pollution
b
Total CVD
mortality (310
3
)
CEV
(310
3
)
IHD
(310
3
)
CVD
c
(310
3
)
Other NCD
c
(310
3
)
All diseases
d
(310
3
)
Deaths per
100 000
YLL
(310
6
)
LLE
(years)
Europe 2138 64 313 377 (48%) 255 (32%) 790 133 14 2.2
EU-28 1849 48 216 264 (40%) 249 (38%) 659 129 11.5 2.1
Germany 330 7 42 49 (40%) 48 (39%) 124 154 2.1 2.4
Italy 221 6 23 29 (36%) 35 (43%) 81 136 1.2 1.9
Poland 180 6 27 33 (57%) 13 (22%) 58 150 1.1 2.8
United Kingdom 147 3 14 17 (27%) 29 (45%) 64 98 1.1 1.5
France 144 3 13 16 (24%) 38 (57%) 67 105 1.1 1.6
a
Data for all EU countries, including 95% CI, are given in the Supplementar y material online (overall uncertainty about ±50%).
b
CEV is cerebrovascular disease, IHD is ischaemic heart disease, CVD are total cardiovascular diseases (CEV þIHD), NCD are non-communicable diseases. YLL are years of
life lost. LLE is loss of life expectancy.
c
Percentages refer to fractional contributions of CVD and other NCD to attributable mortality from all diseases.
d
All diseases refer to NCD þLRI according to Burnett et al.
13
Excess deaths (1000 km2)
< 0.1
1
10
100
> 1000
Figure 2 Regional distribution of estimated annual excess
mortality rates from cardiovascular diseases (CVD = IHD þCEV)
attributed to air pollution. These rates are lower limits as other
non-communicable diseases are not included.
Figure 3 Estimated annual excess mortality rates attributed to air
pollutionin the EU-28 for lower respiratory tract infections, chronic
obstructive pulmonary disease, lung cancer, cerebrovascular dis-
ease, ischaemic heart disease, and other non-communicable dis-
eases. Bars compare results from the Global Burden of Disease
(2015) and the new GEMM. CEV, cerebrovascular disease; COPD,
chronic obstructive pulmonary disease; EU-28, 28 countries of the
European Union; GBD, Global Burden of Disease; GEMM, Global
Exposure Mortality Model; IHD, ischaemic heart disease; LC, lung
cancer; LRI, lower respiratory tract infections; NCD, non-commu-
nicable diseases.
CVD burden from ambient air pollution in Europe 1593
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the total estimated excess mortality rate is 790 000 (95% CI
645 000–934 000) per year in Europe (Figure 4), and 659 000 (95%
CI 537 000–775 000) per year in the EU-28. The European
Environment Agency
18
acknowledges about 400 000/year for the
EU-28, which thus needs to be revised substantially upward. Our
results indicate that the contribution by CVD alone in the EU-28 is
264 000 per year, and potentially up to 513 000 per year if we include
the other NCD, albeit with substantial uncertainty. This adds weight
to the special report of the European Court of Auditors, which
affirms that health within the EU-28 is insufficiently protected.
19
The
report states that ‘European citizens still breathe harmful air, mostly
due to weak legislation and poor policy implementation’.
The major impact of air pollution on CVD is illustrated by Figure 5,
showing the ratio between the attributable excess mortalities related
to CVD (IHD þCEV) and respiratory diseases (RD = LRI þCOPD
þLC). On average, this ratio is close to two in Europe and the EU-
28; and it would be about twice as high if the other NCD would be
included. While the respiratory system acts as ‘gatekeeper’ between
polluted air and the human body, being directly affected through RD,
even greater harm is done through CVD. Figure 5also shows a re-
markable west-east gradient in the CVD/RD ratio, being an order of
magnitude higher in eastern than in western Europe. Since this gradi-
ent does not correspond to a similar gradient in air pollution expos-
ure, it may be explained by more advanced health care in western
Europe, where life expectancy is generally higher. Obviously, both
health care and air quality can be limiting factors.
The EU applies an annual mean air quality limit of 25 mg/m
3
for
PM
2.5
since 2015, which is 2.5 times higher thanthe guideline concen-
tration of 10 mg/m
3
of the WHO. Figure 1shows that even at 10 mg/
m
3
hazard ratios significantly exceed 1.0, both for the GEMM and the
GBD 2015, while especially for IHD they increased substantially with
the GEMM. Clearly, hazard ratios are high at 25 mg/m
3
, e.g. about 1.5
for IHD (Figure 1), indicating that the EU-28 air quality standard is in-
sufficient. For comparison, in the USA, the annual mean limit is 12 mg/
m
3
(since 2012), and in Canada 10 mg/m
3
since 2015, to be reduced
to 8.8 mg/m
3
in 2020. In Australia, the annual PM
2.5
limit is 8 mg/m
3
with the goal to further reduce to 7 mg/m
3
in 2025. The EU has for-
mulated exposure reduction targets for 2020, associated with an an-
nual PM
2.5
level of 20 mg/m
3
. However, even the current limit is
exceeded in several parts of Europe.
20
Clearly, additional efforts are
needed to warrant clean air.
Cardiovascular disease associated with
PM
2.5
It is generally accepted that chronic effects of air pollution on cardio-
vascular events are larger than acute effects, and that elderly and indi-
viduals with prior CVD or associated factors are at higher risk.
11
An
increase of 10 mg/m
3
in annual mean PM
2.5
is associated with a signifi-
cantly enhanced risk for hospitalizations and heart failure mortality.
21
There is ample evidence of adverse health effects from PM
2.5
at con-
centrations below current standards in the USA.
22
Numerous studies
have established a strong association between air pollution and car-
diovascular events, such as myocardial infarction, stroke, heart failure
(including hospitalization for acute left heart decompensation), ar-
rhythmia, and venous thromboembolism (for reviews, see refs
5,11,23
)
The ESCAPE project established a 13% increase in non-fatal acute
coronary events from the long-term exposure to PM
2.5
at 5 mg/m
3
elevation.
24
Recent evidence indicates an excess risk of acute
Figure 4 Estimated excess mortality attributed to air pollution in
Europe, and the contributing disease categories. At least 48% are
due to cardiovascular disease (ischaemic heart disease and stroke).
A fraction of other non-communicable diseases should also be
counted to cardiovascular diseases related mortality, with an upper
limit of 32%. COPD, chronic obstructive pulmonary disease.
CVD excess deaths / RD excess deaths
0.7
0.8
0.9
1
1.5
2
3
4
5
6
7
8
9
10
15
Figure 5 Ratio between attributable excess mortalities related to
cardiovascular diseases and to respiratory diseases (including lung
cancer) for different countries. The calculated ratios are lower limits
as other non-communicable diseases are not included. CVD, car-
diovascular diseases; RD, respiratory diseases.
1594 J. Lelieveld et al.
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coronary syndrome in response to PM
2.5
exposure in subjects with
angiographically diagnosed coronary artery disease.
20
We find that the number of CVD deaths attributable to air pollu-
tion is higher than expected, which may be explained by adverse
effects on other NCD such as diabetes and hypertension. This is sup-
ported by two recent meta-analyses, which calculated a substantially
increased risk for diabetes mellitus Type 2 per 10mg/m
3
increase of
PM
2.5
.
23,25
Further, the enhanced exposure to PM
2.5
by 10 mg/m
3
leads to an increase of systolic and diastolic blood pressure by
1–3 mmHg and is associated with a hazard ratio of 1.13 for the devel-
opment of arterial hypertension.
26,27
Fine particulate matter has been
shown to cause vascular (endothelial) dysfunction by activating mo-
lecular pathways leading to increased oxidative stress
11
through
mechanisms that are strikingly similar to those underlying vascular
dysfunction established in the setting of diabetes
28
and hyperten-
sion.
29
Therefore, it appears that air pollution triggers and/or aggra-
vates other NCD, such as diabetes and hypertension, which may
significantly contribute to CVD outcomes.
Emission control—an effective
intervention
While it is desirable to reduce annual mean PM
2.5
pollution well
below 10 mg/m
3
(the safe threshold is around 2–3 mg/m
3
), in reality
there are limitations to what is achievable, in part because some
PM
2.5
is natural. We performed sensitivity calculations by assuming a
phase-out of fossil fuel related emissions (needed to achieve the 2C
climate change goal under the Paris Agreement). The calculations in-
dicate that in Europe an excess mortality rate of 434 000 (95% CI
355 000–509 000) per year could be avoided by removing fossil fuel
related emissions. About 80% of the avoided European mortality is
within the EU-28. The increase in mean life expectancy in Europe
would be 1.2 (95% CI 1.0–1.4) years. It follows that the switch from
fossil to clean, renewable energy sources is a highly effective health
promotion intervention. The European attributable mortality rate
would decrease by about 55%. This is a tremendous health co-
benefit from the phase-out of carbon dioxide emissions.
Limitations
Figure 1illustrates the higher hazard ratios of the GEMM compared
with the last GBD estimates, especially for IHD, including uncertainty
ranges (95% CI).
8,13
It should be emphasized that the 95% CI refers
to statistical uncertainty associated with the epidemiological data, and
not methodological uncertainty, including unaccounted confounding
factors, assumptions about counterfactuals or limited representative-
ness of the hazard ratio functions (for details, see Supplementary ma-
terial online). The confounder problem can work in two directions,
either by over-attributing air pollution deaths to disease categories,
or by unaccounted air pollution impacts, e.g. on birth weight and neo-
natal deaths, and diseases that may not be captured under the other
NCD.
3,7
Since the contribution by other NCD has been derived
from the difference between the total and the known NCD the 95%
CI is relatively large, about ±55%, while for the other disease catego-
ries ±10–40% (for Europe). Because it is not possible to unambigu-
ously determine the total uncertainty from epidemiological data
alone, we estimate the overall uncertainty to be larger than the
indicated 95% CI, i.e. about ±50% of the calculated mean values.
7
In
the presentation of our results, however, we follow the GBD con-
vention by reporting the 95% CI.
Future directions
Newby et al.
12
emphasized the abundance of evidence that air pollu-
tion contributes to CVD and associated mortality. Our results indi-
cate a much higher disease burden than previously assumed. It will be
important to reconcile the air pollution-induced mechanisms respon-
sible for relatively well-established causes of CVD and mortality (e.g.
IHD and stroke) and potentially newly identified ones that contribute
to other NCD (e.g. hypertension and diabetes). Furthermore, there
is still little mention of air pollution as a risk factor in the European
and American guidelines on health care and disease prevention.
While the clinical practice guidelines of the European Society of
Cardiology indicate that air pollution can adversely affect cardiovas-
cular health, we propose to additionally include recommendations
on the mitigation of risks by individuals, organizations or
governments.
30
Conclusions
BycombiningthenewGEMMofBurnettet al.,
13
which is based on an
unmatched large number of cohort studies, with global air pollution
exposure data,
7
we estimate that the attributable excess mortality
rate is about 8.79 million per year with an overall uncertainty of about
±50%. It is associated with a mean LLE of 2.2 years in Europe. In the
EU-28 alone, between 15% and 28% of the total CVD mortality of
1.85 million/year is attributable to air pollution, the upper limit being
associated with ‘other NCD’, though with substantial uncertainty. By
considering the general pathways of how air pollution causes vascular
impairment, the actual percentage may be closer to the upper than
the lower limit, indicating that it may be higher than 20%, and suggest-
ing that that air pollution is a health risk factor that may exceed that
of tobacco smoking. We conclude that improving European air qual-
ity is an achievable, highly effective, and therefore imperative health
promotionintervention. By replacing fossil energy sources with clean,
renewable fuels, needed to meet the goals of the Paris Agreement on
climate change, the attributable mortality rate in Europe could be
reduced by 55%. Further reductions are feasible by additionally con-
trolling other industrial and agricultural pollution sources.
Supplementary material
Supplementary material is available at European Heart Journal online.
Acknowledgements
We thank the Mainz Heart Foundation for continuous support. T.M.
is PI of the DZHK (German Center for Cardiovascular Research),
Partner Site Rhine-Main, Mainz, Germany. We also thank the
International Scientific Partnership Program (ISPP) of the King Saud
University for supporting the research.
Conflict of interest: none declared.
CVD burden from ambient air pollution in Europe 1595
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Chapter
In recent years, to deal with the accelerating adverse impacts of climate change and resource exploitation caused by human activities, new concepts of economic development are emerging and discussed around the world. Among them, “green economy” is the most comprehensive term and well-accepted concept that is directly related to the Sustainable Development Goals of the United Nations (SDGs). With the mission to eliminate the externalities of industry or human development, green economy has developed many mechanisms to regulate economic behaviors or lead industry to sustainable production and innovative business models such as the financial schemes of carbon tax and financial subsidy. In the international society, the environment and trade negotiations around the world are concurrently undergoing. The Organisation for Economic Co-operation and Development (OECD) is also promoting Green Growth as the strategy for green economy while the United Nations Environmental Programme (UNEP) is advocating “Green New Deal.” The common objective of these policies and programs is to overcome environmental crisis such as climate change but also maintain global productivity. On the domestic side, the production and implementation of green products and services are also being promoted and encouraged through different schemes by governments in order to fulfill their obligations of carbon emission reduction. While environmental protection and economic development have been long contradictive to each other in human societies. Once the green industry or greener production can be developed, the status of green economy can step forward in the future.
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Ambient air pollution is a leading cause of non-communicable disease globally. The largest proportion of deaths and morbidity due to air pollution is now known to be due to cardiovascular disorders. Several particulate and gaseous air pollutants can trigger acute events (e.g. myocardial infarction, stroke, heart failure). While the mechanisms by which air pollutants cause cardiovascular events is undergoing continual refinement, the preponderant evidence support rapid effects of a diversity of pollutants including all particulate pollutants (e.g. course, fine, ultrafine particles) and gaseous pollutants such as ozone, on vascular function. Indeed alterations in endothelial function seem to be critically important in transducing signals and eventually promoting cardiovascular disorders such as hypertension, diabetes, and atherosclerosis. Here, we provide an updated overview of the impact of particulate and gaseous pollutants on endothelial function from human and animal studies. The evidence for causal mechanistic pathways from both animal and human studies that support various hypothesized general pathways and their individual and collective impact on vascular function is highlighted. We also discuss current gaps in knowledge and evidence from trials evaluating the impact of personal-level strategies to reduce exposure to fine particulate matter (PM2.5) and impact on vascular function, given the current lack of definitive randomized evidence using hard endpoints. We conclude by an exhortation for formal inclusion of air pollution as a major risk factor in societal guidelines and provision of formal recommendations to prevent adverse cardiovascular effects attributable to air pollution.
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ABI : ankle–brachial (blood pressure) index ABPM : ambulatory blood pressure monitoring ACCORD : Action to Control Cardiovascular Risk in Diabetes ACE-I : angiotensin-converting enzyme inhibitor ACS : acute coronary syndromes ADVANCE : Action in Diabetes and Vascular disease: PreterAx
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Fine particulate matter <2.5 μm (PM2.5) air pollution is the most important environmental risk factor contributing to global cardiovascular (CV) mortality and disability. Short-term elevations in PM2.5 increase the relative risk of acute CV events by 1% to 3% within a few days. Longer-term exposures over several years increase this risk by a larger magnitude (∼10%), which is partially attributable to the development of cardiometabolic conditions (e.g., hypertension and diabetes mellitus). As such, ambient PM2.5 poses a major threat to global public health. In this review, the authors provide an overview of air pollution and health, including assessment of exposure, impact on CV outcomes, mechanistic underpinnings, and impact of air pollution reduction strategies to mitigate CV risk. The review concludes with future challenges, including the inextricable link between air pollution and climate change, and calls for large-scale trials to allow the promulgation of formal evidence-based recommendations to lower air pollution–induced health risks.
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