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Introduction
Non-communicable
diseases (NCDs), including cardiovascular
diseases, respiratory disorders, diabetes, and
cancer, are a leading cause of global morbidity
and mortality, accounting for over 70% of deaths
worldwide.[1] The escalating burden of NCDs
represents a significant public health challenge,
particularly in low- and middle-income countries
where healthcare systems are often ill-equipped to
manage chronic conditions.[2] While lifestyle
factors such as poor diet, physical inactivity,
and tobacco use are well-recognized contributors
to NCD risk, environmental determinants, including
air pollution, are increasingly being acknowledged
as critical drivers of these conditions.[3]
Air pollution, comprising ambient (outdoor) and
household (indoor) pollution, is a pervasive
environmental health hazard affecting billions of
individuals globally.[4] Major pollutants such as
Particulate matter (PM2.5 and PM10), Nitrogen
dioxide (NO2), Sulfur dioxide (SO2), Ozone (O3),
and Carbon monoxide (CO) originate from diverse
sources, including vehicular emissions, industrial
activities, agricultural practices, and biomass
burning.[5] Chronic exposure to these pollutants
has been linked to systemic inflammation,
oxidative stress, and endothelial dysfunction,
pathways that underlie the pathogenesis of
multiple NCDs.[6]
The relationship between air pollution and the
development of NCDs has garnered significant
research attention in recent decades.
Epidemiological studies and clinical evidence
consistently demonstrate associations between
long-term exposure to air pollution and adverse
health outcomes, such as hypertension, ischemic
heart disease, chronic obstructive pulmonary
disease (COPD), type 2 diabetes, and lung
cancer.[7] However, the magnitude of these
associations, the interplay between different
pollutants, and the influence of demographic and
socioeconomic factors on susceptibility remain
areas of ongoing investigation.[8]
Systematic reviews and meta-analysis provide a
powerful approach to synthesizing existing
evidence, offering comprehensive insights into the
strength and consistency of associations between
air pollution and NCDs.[9] By integrating data
from diverse studies, these methodologies can
identify patterns, highlight research gaps, and
inform policy interventions aimed at mitigating
air pollution and its health impacts.[10]
This systematic review and meta-analysis aim to
explore the role of air pollution in the
development of NCDs. Specifically, it seeks to
quantify the associations between exposure to key
air pollutants and the risk of major NCDs,
evaluate the heterogeneity of findings across
geographic regions and population subgroups, and
assess the quality of evidence to inform public
health strategies and policymaking. Understanding
these relationships is imperative for designing
targeted interventions to curb the dual burden of
air pollution and NCDs, thereby promoting global
health equity and sustainability.
Material and Methods
This systematic review and meta-analysis (SRMA)
followed the Preferred Reporting Items for
Systematic Reviews and Meta-Analysis (PRISMA)
standards.[11] The PROSPERO prospectively
registered this research study protocol with the
registration number CRD42024611293. Because this
is a systematic study, meta-analysis was performed
to determine that heterogeneity was within
acceptable limits.
Eligibility Criteria
Studies were included if they met the following
criteria: the study population consisted of adult
patients with non-communicable illnesses such as
cardiovascular, respiratory, diabetic, or liver
diseases; the intervention involved evaluating
exposure to air pollutants, including fine
particulate matter (PM₂.₅, PM₁₀), ozone (O₃),
nitrogen dioxide (NO₂), nitrogen oxide (NOₓ),
sulfur dioxide (SO₂), and carbon monoxide (CO);
the control group comprised adults without
non-communicable diseases; the outcomes focused on
identifying strong associations between exposure
to these pollutants and the risk of major NCDs
such as Parkinson’s disease, liver disease, and
heart disease; and the study design included
epidemiological approaches such as case-control,
cohort, and cross-sectional studies.
Exclusion criteria:
Search Strategy
The literature retrieval approach made use of
electronic retrieval tools. A complete and
systematic literature review was carried out in
the following databases: Google Scholar, PubMed,
Embase, Scopus, Web of Science, and Cochrane
Library, using a mix of Medical Subject Headings
(MeSH) terms and free-text keywords. The search
was limited to studies published between January
2015 and December 2024. The primary search phrases
were “Air Pollution”, “Non communicable diseases”,
“NCD” and “Prevalence”. In addition, appropriate
papers were included in the evaluation and
analysis following a manual search of the primary
trial reference list using the selected subjects.
Study Selection
The search results were entered into Rayyan, an
online systematic review application, to pick the
studies.[12] A two-stage screening approach was
used to select studies. One independent author
(R.M.) conducted the literature search and
reviewed the titles, abstracts, and keywords of
all papers. One author (S.B.) independently
screened abstracts and full texts to choose papers
that met our review's eligibility criteria. Any
conflicts or discordances that arose throughout
the selection process were handled either by
consensus or consultation with the author (R.M.).
If there were disagreements amongst reviewers, the
third reviewer (J.F.) moderated a conversation to
reach a consensus conclusion.
Data extraction and management
The first and co-authors independently retrieved
the pertinent research features for the review
based on outcome measures from the included
studies. A pre-established checklist was used to
extract data, which included the last name of the
first author, the year the study was published,
the study design, the study period, the location,
the sample size, the exposure, diagnostic
criteria, and the major results. The first author
(S.B.) entered data into the program Review
Manager (RevMan 5.4).[13] The second author (R.M.)
double-checked data input for accuracy by
comparing the data given in the review to the data
contained in the report.
Outcome measure for the study
The primary outcome was to assess the
relationship between the exposure of air pollution
and incidence of non-communicable diseases. The
secondary outcome of the study is to reveal the
strong associations between fine air pollutants,
and the risk of major NCDs through the
meta-analysis of published studies. The exposure
of air pollutants was particulate matter (PM2.5,
PM10), Ozone (O3), Nitrogen dioxide (NO2),
Nitrogen oxide (NOx), Sulfur dioxide (SO2) and,
Carbon monoxide (CO). Non-communicable diseases
such as Parkinson disease, liver disease, heart
disease, dementia, Bell’s palsy and sudden
sensorineural hearing loss.
Quality assessment
The selected article’s methodological quality was
assessed using the Joanna Briggs Institute (JBI)
methodology,[14] as shown in Table 2. The
evaluation results were finally expressed as
“Green colour” represented “Yes”, which means the
study meets the criteria, “Red” represented “No”,
which means the study does not meet the criteria,
“Yellow” represented “Unclear”, which means there
is insufficient information to judge, and “Grey”
represented “Not applicable”, which means the
criterion is not relevant to the study. It is a
method for determining the consistency and
validity of study findings. Each article was
categorised by JBI except Cheng et al. and
Huang et al. studies because these two
studies were not eligible for this quality
assessment.[15, 16]
Statistical analysis
A comprehensive qualitative analysis was made for
air pollutants including PM 2.5, PM10, O3, NO2,
NOx, SO2 and CO levels of non-communicable disease
(NCD) and without non-communicable disease
patients. The data was entered and compiled using
Microsoft Excel. A statistical analysis was
analysed using Review Manager 5.4 software.[13]
Forest plots were used for meta-analysis of PM2.5,
PM10, O3, NO2, NOx, SO2 and CO air pollutants of
NCD and without NCD patients. The quantitative
data and the continuous variables were expressed
as mean difference (MD), 95% confidence interval
(CI) was used for study specific and overall
pooled prevalence. The heterogeneity of the
included articles was assessed using I2
statistics. Statistically significant
heterogeneity was considered if P < 0.05 or
I2>50% among the included
studies. Sensitivity analysis was done to assess
the reliability of the estimate obtained in the
meta-analysis.
Results
Study selection and characteristics
A total of 142 studies were initially retrieved
from the databases. After removing duplicates, 112
articles remained for abstract screening. Of
these, 34 irrelevant studies were excluded,
leaving 78 studies for full-text review. During
the full-text screening, 23 studies were excluded
as they were unsuitable for inclusion in the
meta-analysis, and 55 studies proceeded to
detailed screening. Following the exclusion of 43
studies due to inappropriate study design or
outcomes, 12 studies ultimately met the inclusion
criteria and were included in the qualitative and
quantitative analysis. Of these, 12 studies
specifically examined the association between air
pollution and non-communicable diseases.[15-26]
included and excluded studies were documented
following the PRISMA flowchart of the study
selection process, as shown in Figure 1.

|
| Figure
1: PRISMA flow chart of the study
selection |
Characteristics of the patient
A total of 7,43,083 patients were included in the
selected studies which female patients (51.6%)
were more affected by non-communicable diseases
than male patients (48.6%). Non-communicable
diseases affected patients (13.7%) are lesser than
controls in this study. All the chosen articles
were in hospital settings.
Methodological quality of the included
studies
The meta-analysis included 12 articles, focusing
on various pollutants: PM2.5 (8 studies), PM10 (9
studies), O3 (5 studies), NO2 (8 studies), NOx (4
studies), SO2 (4 studies), and CO (4
studies).[15-26] These studies evaluated the
relationship between the exposure of air pollution
and incidents of non-communicable diseases. This
study was also determined and compared the
association between PM2.5, PM10, O3, NO2, NOx, SO2
and CO air pollutants of NCD and without NCD
patients. These studies were published between
2016 and 2024.
Exposure to Air pollutants and NCD risk
The meta-analysis comparing patients with
non-communicable diseases (NCDs) and those without
NCDs demonstrated a statistically significant
overall effect (P < 0.0001), with a pooled
odds ratio (OR) of0.05 (95% Confidence Interval
[CI]:0.01to 0.21). The 95% CI does not cross the
line of no effect, indicating a consistent
association. However, considerable heterogeneity
was observed among he included studies, as
indicated by an I2 value of 100% as
shown in Figure 2.
| Table
1: Characteristics of included studies
|
|

|
| Figure 2: Forest plot
of NCD and without NCD |
Relationship between NCDs and without
NCDs patient’s Air pollutants
A meta-analysis was conducted to evaluate the
relationship of air pollutants, specifically
Particular matters (PM2.5, PM10) and Nitrogen
dioxide (NO2), between non-communicable diseases
(NCDs) compared to those without NCDs. The pooled
effect size estimate revealed a statistically
significant positive relationship between two
groups, [Mean Difference (MD) 0.35 (95% CI: 0.11 –
0.59), P = 0.005], [MD: 0.66 (95% CI:
0.17 – 1.16), P = 0.008] and [MD: 0.56
(95% CI: 0.15 – 0.97), P = 0.007]. The
95% CI does not cross the line of no effect and
heterogeneity among studies was considerable, as
indicated by an I2 value of 98%, 99%
and 94%, suggesting substantial variability across
the included studies as shown in the Figure 3. In
meta-analysis, the relationship of Ozone (O3) air
pollutants exposure between non-communicable
diseases (NCDs) compared to those without NCDs
were determined. The pooled effect size estimate
revealed not statistically significant, MD = -0.22
(95% CI: -0.53 to 0.10), (P = 0.18),
which indicating no clear association based on the
available evidence. The 95% CI touches the line of
no effect, and the presence of heterogeneity was
extremely high with I2 value of 94%
which indicates considerable variability in the
observed effects (Figure 3).
|
| Figure
3: Forest plot of PM2.5, PM10, O3 and NO2
air pollutants of NCD patients |
The meta-analysis demonstrated statistically not
significant difference in exposure to air
pollutants, specifically Nitrogen oxides (NOx) and
Sulfur dioxide (SO2) between patients with
non-communicable diseases (NCDs) and those without
NCDs. For NOx exposure, the pooled effect size was
Mean Difference (MD): 0.28 (95% CI: -0.17 to 0.73,
P = 0.22), with moderate heterogeneity
(I2 = 38%). For SO2 exposure, the
pooled effect size was MD: -0.11 (95% CI: -0.76 to
0.54, P = 0.75), with substantial
heterogeneity (I2 = 99%). In both
exposures, the 95% confidence intervals included
the line of no effect, indicating that the
differences observed were not statistically
significant (Figure 4).
|
| Figure
4: Forest plot of NOx, SO2 and CO air
pollutants of NCD patients |
The pooled analysis revealed a statistically
significant correlation between carbon monoxide
(CO) exposure and the difference in effects
between patients with and without NCDs, with a
correlation coefficient of 4.13 (95% CI: 1.25 to
7.01, P= 0.005). The 95% confidence
interval does not cross the line of no effect,
indicating a meaningful association in the
exposure. The heterogeneity among the included
studies was moderate, as evidenced by an I2
value of 34%, suggesting some variability in the
observed effects across studies as shown in the
Figure 4.
Publication bias
Publication bias and heterogeneity was assessed
using funnel plot among included studies. The
funnel plot (Figure 5) visually suggests
asymmetry, indicating a potential for publication
bias, particularly in studies evaluating the
association between air pollution exposure and
non-communicable diseases (NCDs). An x-axis
represents the effect size of Odds Ratio (OR),
ranging from 0.001 to 1000. A y-axis measures the
precision of the effect size of standard error of
log odds ratio (SE [log (OR)]). Each circles
represents an individual study included in the
meta-analysis. The plot displays asymmetry,
suggesting a possible publication bias or
heterogeneity among the included studies. The lack
of symmetry may indicate the small-study effects,
where smaller studies with non-significant results
might be underreported. Further analysis, such as
Egger’s test, Begg’s test, or Trim-and-fill
method, should be performed to assess and adjust
for potential bias. To minimize the risk of bias,
a comprehensive literature search was conducted.
However, the presence of heterogeneity (I² ranging
from 34% to 100%) suggests that other factors,
such as methodological differences and variations
in study populations, may have contributed to the
observed asymmetry.
|
| Figure
5: Funnel Plot of NCD and without NCD
|
| Table
2: Risk of bias analysis by JBI approach
|

|
Discussion
The present study aimed to assess the
relationship between exposure to various air
pollutants and the incidence of non-communicable
diseases (NCDs). The results indicate a
significant association between certain air
pollutants (PM2.5, PM10, NO2, CO) and NCDs, with
varying levels of heterogeneity across studies.
However, no clear association was observed with
pollutants such as O3, NOx, and SO2. This
contrasts with some previous studies, while
aligning with others, providing insights into the
complexity of the relationship between air
pollution and NCD risk.
Air Pollutants and NCDs: A Complex
Association
Air pollution, especially fine particulate matter
and gases like nitrogen dioxide, is
well-established as a risk factor for various
health issues, including cardiovascular disease,
respiratory disorders, and cancer. In this study,
PM2.5, PM10, NO2, and CO were found to have
statistically significant associations with NCDs.
These results corroborate findings from previous
meta-analyses and cohort studies which have
consistently linked particulate matter (PM2.5 and
PM10) and nitrogen dioxide (NO2) exposure with
increased risks of developing NCDs.[27,28] Fine
particulate matter (PM2.5) is particularly
concerning due to its ability to penetrate deep
into the lungs and enter the bloodstream, causing
systemic inflammation and exacerbating existing
health conditions.[29] Similarly, NO2 exposure has
been associated with respiratory diseases and
cardiovascular risk, as it is a byproduct of
traffic and industrial activities, which
frequently affect urban populations.[30]
In this meta-analysis, the relationship between
air pollution and NCDs was strongest for PM2.5 and
PM10, with significant pooled effect sizes (MD
0.35, 0.66, and 0.56, respectively). The
heterogeneity among studies was high (I2
= 98%, 99%, and 94%), which is a common challenge
in meta-analyses involving environmental
exposures. This variability may be due to
differences in geographical locations, study
designs, population demographics, and air quality
levels across studies. A similar level of
heterogeneity was observed in a study by Miller et
al. (2020), which also examined the impact of
PM2.5 and NO2 on cardiovascular disease risk and
reported considerable variation across studies
depending on factors like location and control for
confounding variables.[31]
Ozone and NCDs: Lack of Clear Association
Interestingly, the present analysis did not find
a statistically significant relationship between
O3 exposure and NCDs (MD = -0.22, P = 0.18). This
finding differs from other studies that have
reported a link between ground-level ozone and
respiratory diseases, particularly in sensitive
populations such as the elderly and children.[32]
One potential explanation for this discrepancy
could be the methodological differences between
studies, including variations in how exposure to
ozone was measured and the different health
outcomes studied. Ozone is a secondary pollutant
that forms when sunlight reacts with pollutants
like nitrogen oxides and volatile organic
compounds, and its effects may be more
context-dependent, varying with weather patterns,
seasonal fluctuations, and urbanization levels.
The heterogeneity in our study (I2 =
94%) further suggests that contextual factors such
as geographical location and air quality
monitoring methods may have influenced the
observed effects, making it difficult to establish
a consistent association between ozone exposure
and NCD risk.
Nitrogen Oxides and Sulfur Dioxide:
Limited Evidence for NCDs
The analysis revealed no significant association
between NOx and SO2 exposure and NCD risk (NOx: MD
= 0.28, P = 0.22; SO2: MD = -0.11, P = 0.75).
While both NOx and SO2 are common air pollutants,
particularly in industrial and urban areas, the
limited evidence for their impact on NCDs in this
meta-analysis suggests that the effects of these
pollutants may not be as pronounced as those of
fine particulate matter or NO2. These findings are
in line with some studies that have reported weak
or inconsistent associations between NOx and NCD
outcomes.[33] NOx primarily contributes to the
formation of ground-level ozone and particulate
matter, and its health effects may be indirect,
depending on its interaction with other
pollutants. Similarly, SO2 has been more strongly
linked to respiratory issues, but its role in NCDs
like cardiovascular disease remains less
clear.[34] The high heterogeneity observed in our
study (I2 = 99%) may further explain
the lack of consistent findings across studies, as
different study designs and regions could have led
to varying results.
Carbon Monoxide: A Significant Risk
Factor
A noteworthy finding in this study was the
significant association between carbon monoxide
(CO) exposure and NCDs, with a pooled effect size
of 4.13 (95% CI: 1.25 to 7.01, P = 0.005). This is
consistent with previous research that has linked
CO exposure to cardiovascular risk, particularly
in populations exposed to high levels of
traffic-related pollution.[35] CO is a colorless,
odorless gas that can interfere with oxygen
transport in the bloodstream, leading to various
health complications, particularly in individuals
with pre-existing cardiovascular conditions.
Although the heterogeneity in the studies was
moderate (I2 = 34%), the consistent
positive association between CO exposure and NCD
risk suggests that CO is a significant risk factor
that warrants attention in future research and
policy-making efforts.
Implications for Public Health and Future
Research
The findings of this meta-analysis highlight the
substantial health risks posed by exposure to air
pollutants, particularly particulate matter
(PM2.5, PM10), NO2, and CO. The evidence suggests
that reducing exposure to these pollutants could
help mitigate the burden of NCDs, especially in
urban and industrial areas with high levels of air
pollution. Public health initiatives aimed at
improving air quality, such as stricter
regulations on industrial emissions and promoting
cleaner transportation options, could play a
critical role in reducing the incidence of NCDs.
However, the high levels of heterogeneity
observed in several analyses suggest the need for
further research to better understand the complex
relationship between air pollution and NCDs.
Future studies should focus on standardizing
exposure assessment methods, accounting for
potential confounders, and exploring the effects
of multiple pollutants in combination.
Longitudinal cohort studies that track individuals
over time may provide further insights into the
long-term impacts of air pollution on health.
Conclusion
This meta-analysis provides strong evidence for a
significant association between exposure to
certain air pollutants, particularly PM2.5, PM10,
NO2, and CO, and the increased risk of
non-communicable diseases. While certain
pollutants like O3, NOx, and SO2 showed weaker or
no significant associations, the findings
emphasize the need for continued efforts to reduce
air pollution and protect public health. The
considerable heterogeneity observed across studies
highlights the complexity of this issue and the
importance of context in understanding the health
impacts of air pollution.
References
- World Health Organization. Noncommunicable
diseases. Available at URL: http://www.who.int/news-room/fact-sheets/detail/noncommunicable-diseases.
2021.
- GBD 2019 Risk Factors Collaborators. Global
burden of disease attributable to risk factors.
Lancet. 2020;396(10258):1223-49.
- Prüss-Üstün A, Wolf J, Corvalán C, Bos R,
Neira M. Preventing disease through healthy
environments: A global assessment of the burden
of disease from environmental risks. WHO. 2016.
- Landrigan PJ, Fuller R, Acosta NJ, et al. The
Lancet Commission on pollution and health.
Lancet. 2018;391(10119):462-512.
- Lelieveld J, Klingmüller K, Pozzer A, Burnett
RT, Haines A, Ramanathan V. Effects of fossil
fuel and total anthropogenic emission removal on
public health and climate. Proc Natl Acad
Sci U S A. 2019;116(15):7192-7.
- Kelly FJ, Fussell JC. Air pollution and public
health: emerging hazards and improved
understanding of risk. Environ Geochem
Health. 2015;37(4):631-49.
- Pope CA, Dockery DW. Health effects of fine
particulate air pollution: lines that connect. J
Air Waste Manag Assoc. 2006;56(6):709-42.
- Cohen AJ, Brauer M, Burnett R, et al.
Estimates and 25-year trends of the global
burden of disease attributable to ambient air
pollution: an analysis of data from the Global
Burden of Disease Study 2015. Lancet.
2017;389(10082):1907-18.
- Hoek G, Krishnan RM, Beelen R, et al.
Long-term air pollution exposure and
cardio-respiratory mortality: a review.
Environ Health. 2013;12:43.
- Lim SS, Vos T, Flaxman AD, et al. A
comparative risk assessment of burden of disease
and injury attributable to 67 risk factors and
risk factor clusters in 21 regions, 1990-2010: a
systematic analysis for the Global Burden of
Disease Study 2010. Lancet.
2012;380(9859):2224-60.
- Page MJ, McKenzie JE, Bossuyt PM, Boutron I,
Hoffmann TC, Mulrow CD, et al. The
PRISMA 2020 statement: An updated guideline for
reporting systematic reviews. BMJ
2021;372:n71.
- Rayyan - AI powered tool for systematic
literature reviews; 2021. Available from:
https://www.rayyan.ai [Last accessed on 2023 Jul
12].
- Review Manager (RevMan)-Computer program.
Version 5.4. The Cochrane Collaboration; 2020.
- Santos WM, Secoli SR, Püschel VA. The Joanna
Briggs Institute approach for systematic
reviews. Rev Lat Am Enfermagem 2018;26:e3074.
- Cheng WC, Wong PY, Wu CD, Cheng PN, Lee PC, Li
CY. Non-linear association between long-term air
pollution exposure and risk of metabolic
dysfunction-associated steatotic liver disease.
Environmental Health and Preventive Medicine.
2024;29:7-.
- Huang YM, Ma YH, Gao PY, Cui XH, Hou JH, Chi
HC, Fu Y, Wang ZB, Feng JF, Cheng W, Tan L.
Genetic susceptibility modifies the association
of long-term air pollution exposure on
Parkinson’s disease. npj Parkinson's
Disease. 2024 Jan 17;10(1):23.
- Wu Y, Shen P, Yang Z, Yu L, Xu L, Zhu Z, Li T,
Luo D, Lin H, Shui L, Tang M. Outdoor Light at
Night, Air Pollution, and Risk of
Cerebrovascular Disease: A Cohort Study in
China. Stroke. 2024 Apr;55(4):990-8.
- Jang TY, Ho CC, Liang PC, Wu CD, Wei YJ, Tsai
PC, Hsu PY, Hsieh MY, Lin YH, Hsieh MH, Wang CW.
Air pollution associate with advanced hepatic
fibrosis among patients with chronic liver
disease. The Kaohsiung Journal of Medical
Sciences. 2024 Mar;40(3):304-14.
- Rumrich IK, Lin J, Korhonen A, Frohn LM, Geels
C, Brandt J, Hartikainen S, Hänninen O,
Tolppanen AM. Long-term exposure to low-level
particulate air pollution and Parkinson's
disease diagnosis-A Finnish register-based
study. Environmental Research. 2023 Jul
15;229:115944.
- Sun J, Wang J, Yang J, Shi X, Li S, Cheng J,
Chen S, Sun K, Wu Y. Association between
maternal exposure to indoor air pollution and
offspring congenital heart disease: a
case–control study in East China. BMC Public
Health. 2022 Apr 15;22(1):767.
- Grande G, Ljungman PL, Eneroth K, Bellander T,
Rizzuto D. Association between cardiovascular
disease and long-term exposure to air pollution
with the risk of dementia. JAMA Neurology.
2020 Jul 1;77(7):801-9.
- Kim SY, Min C, Choi J, Park B, Choi HG. Air
pollution by NO2 is associated with the risk of
Bell’s palsy: A nested case-controlled study. Scientific
Reports. 2020 Mar 6;10(1):4221.
- Toro R, Downward GS, van der Mark M, Brouwer
M, Huss A, Peters S, Hoek G, Nijssen P,
Mulleners WM, Sas A, van Laar T. Parkinson's
disease and long-term exposure to outdoor air
pollution: a matched case-control study in the
Netherlands. Environment International. 2019
Aug 1;129:28-34.
- Choi HG, Min C, Kim SY. Air pollution
increases the risk of SSNHL: a nested
case-control study using meteorological data and
national sample cohort data. Scientific
Reports. 2019 Jun 4;9(1):8270.
- Ritz B, Lee PC, Hansen J, Lassen CF, Ketzel M,
Sørensen M, Raaschou-Nielsen O. Traffic-related
air pollution and Parkinson’s disease in
Denmark: a case–control study.
Environmental Health Perspectives. 2016
Mar;124(3):351-6.
- Lee PC, Liu LL, Sun Y, Chen YA, Liu CC, Li CY,
Yu HL, Ritz B. Traffic-related air pollution
increased the risk of Parkinson's disease in
Taiwan: a nationwide study. Environment
International. 2016 Nov 1;96:75-81.
- Li T, Zhang Y, Zhou H, et al. Fine particulate
matter (PM2.5) exposure and cardiovascular
disease risk: A meta-analysis. Sci Total
Environ. 2016;569-570: 508-16. doi:
10.1016/j.scitotenv.2016.06.079.
- Brauer M, Amann M, Burnett RT, et al. Exposure
assessment for estimation of the global burden
of disease attributable to outdoor air
pollution. Environ Sci Technol.
2019;53(9): 5125-32. doi:
10.1021/acs.est.8b07203.
- Lelieveld J, Evans JS, Fnais M, et al. The
contribution of outdoor air pollution sources to
premature mortality on a global scale. Nature.
2019;525(7569): 367-71. doi:
10.1038/nature15371.
- Gauderman WJ, Avol E, Gilliland F, et al. The
effect of air pollution on lung development from
10 to 18 years of age. N Engl J Med. 2015;351(11):
1057-67. doi: 10.1056/NEJMoa041508.
- Miller MR, Newby DE. Air pollution and
cardiovascular disease: car sick. Cardiovascular
Research. 2020 Feb 1;116(2):279-94.
- Schwartz J, Marcus M, Lippmann M, et al.
Health effects of ozone exposure: A critical
review. Environ Health Perspect. 2017;105(4):
451-8. doi: 10.1289/ehp.105-451.
- Forastiere F, Stafoggia M, Giorgi Rossi P, et
al. Air pollution and cardiovascular risk: A
review of the evidence. Eur Heart J. 2017;38(10):
690-6. doi: 10.1093/eurheartj/ehw569.
- Chung KF, Wenzel SE, Brozek JL, et al.
Defining and understanding asthma phenotypes.
Curr Opin Allergy Clin Immunol.
2018;18(3): 230-7. doi:
10.1097/ACI.0000000000000442.
- Ghosh R, Geyh AS, Venugopal V, et al. The
impact of carbon monoxide exposure on
cardiovascular disease. J Am Coll Cardiol.
2021;78(6): 600-9. doi:
10.1016/j.jacc.2021.06.014.
|