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The health effects of fine particulate air pollution

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Matthew Loxham at University of Southampton
Matthew Loxham
Donna Davies at University of Southampton
Donna Davies
Stephen Holgate at University of Southampton
Stephen Holgate
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The health effects of fine particulate air pollution
The harder we look, the more we find
Matthew Loxham Biotechnology and Biological Sciences Research Council future leader fellow,
Donna E Davies professor of respiratory cell and molecular biology, Stephen T Holgate clinical
professor
School of Clinical and Experimental Sciences, Faculty of Medicine, University of Southampton, Southampton, UK
Fine particulate matter (PM) of diameter less than 2.5 microns
(PM2.5) is ubiquitous, emanating especially from transport and
combustion sources. Since a seminal 1993 study showing a clear
association between airborne PM2.5 and mortality rates in six
cities in the United States,1 many attempts have been made to
quantify the global annual burden of mortality due to PM2.5—0.8
million in 2005,2 3.15 million in 2015,3 4 and almost 9 million
in 2018.5 This increase reflects not a 10-fold rise in PM2.5
exposure, but improved modelling of PM2.5 concentrations, and
use of real world exposure-response associations incorporating
new data from developing nations, which has led to conclusions
with increased reliability and, unfortunately, of increased
mortality.
PM2.5 has been associated with diseases of the respiratory and
cardiovascular systems, with cardiovascular disease likely
occurring through systemic inflammation and possibly
translocation of particulate matter into the circulation.6 Indeed,
ultrafine particles (<100 nanometres in diameter) have been
found in the brain and heart.7 8 These mechanisms indicate that
effects are not limited to respiratory and cardiovascular systems,
but uncovering new associations could require hypothesis free
analysis of a dataset large enough to achieve sufficient statistical
power.
In a linked study, Yaguang Wei and colleagues (doi:10.1136/
bmj.l6258) report analyses of more than 95 million US hospital
admissions of Medicare beneficiaries and PM2.5 concentrations
on the day before presentation.9 In addition to confirming
previously established associations between short term PM2.5
concentration and respiratory, cardiovascular, and Parkinson’s
disease, and diabetes mellitus, the authors found that each 1
μg/m3 increase in PM2.5 was associated with 2050 extra hospital
admissions, 12 216 days in hospital, and $31m (£24m, €28m)
in care costs, through diseases not previously associated with
PM2.5. These diseases included septicaemia; fluid and electrolyte
disorders; renal failure; and infections of the urinary tract, skin,
and subcutaneous tissue. Taking into account corresponding
values presented for the burden of diseases already associated
with PM2.5 exposure, the burden of these newly associated
diseases represents 31-38% of the total PM2.5 associated effect,
similar to a recent figure for the burden of disease not previously
associated with PM2.5.10 This proportion suggests that current
figures for PM2.5 associated morbidity, which focus on
established disease associations, might be considerable
underestimates.
Crucially for informing policy, these associations remained
even when the analysis was restricted to days when the PM2.5
concentration was below the World Health Organization’s
guideline of 25 μg/m3, confirming the conclusions of other
authors finding no safe lower limit for exposure to PM2.5.11 More
optimistically, even small decreases in PM2.5 concentration could
have substantial benefits over a large population, although
extrapolation to the global population requires caution, because
government funded health insurance in the US, including
Medicare, is skewed towards individuals aged older than 65,
certain ethnic groups, and people on low incomes.12
People on low incomes and ethnic minorities tend to be more
affected than others by equivalent PM exposure,13 and more
exposed overall on both national and international levels.14 15
Air pollution is a global problem and must be tackled as such.
While the WHO is currently revising its guidelines, these are
not legally binding. However, reducing pollutant concentrations
is critical to reducing the incidence and exacerbation of the
myriad conditions that have been associated, with varying
strengths of evidence, with PM and other air pollutants.16 17
Our knowledge of the health effects of PM is still lacking in
many areas—notably the range of disease outcomes associated
with particulates and their causality; and the effects of long term
exposure, indoor exposure, and ultrafine PM. The relative effects
of different PM sources, and any differences between primary
PM (released from source) and secondary PM (formed by
reactions of pollutant gases following release), are also poorly
understood. We urgently need more epidemiological research
to uncover new disease associations and to investigate newly
reported associations, and toxicology research to explore
potential causative mechanisms. Funding streams should also
take account of the cross disciplinary research required for such
studies to be performed. As the burden of disease associated
with pollution becomes more apparent, better awareness among
Correspondence to: M Loxham m.loxham@soton.ac.uk
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health professionals and the public is needed to help prevent
and control pollution associated disease exacerbations, and to
push for policies to reduce emissions.
During the 2008 Beijing Olympics, transport and industrial
restrictions substantially improved air quality, accompanied by
a 46% drop in relative risk of outpatient visits for asthma.18 Such
restrictions are probably unsustainable, but progress has still
been made. Thirteen years after the aforementioned study on
six US cities,1 which highlighted the association between
premature mortality and fine particulate matter, the authors
re-evaluated the situation. In the intervening years, five of the
six cities showed reduced PM2.5 concentrations, and a
proportionate reduction in PM2.5 associated mortality.19
Clearly, there is much still to learn, but we should not mistake
knowledge gaps for paucity of evidence. The sooner we act, the
sooner the world’s population will reap the benefits.
Competing interests: The BMJ has judged that there are no disqualifying financial
ties to commercial companies. The authors declare the following other interests:
ML is funded by a future leader fellowship from the Biotechnology and Biological
Sciences Research Council and a senior research fellowship from the National
Institute for Health Research Southampton Biomedical Research Centre; SH is a
cofounder and non-executive board director of Synairgen, a consultant for Dyson
on air quality issues, a UK Research and Innovation Clean Air Champion and a
member of the Natural Environment Research Council; DD is a cofounder and
shareholder of Synairgen, and is also a consultant to the company. The BMJ policy
on financial interests is here: https://www.bmj.com/sites/default/files/attachments/
resources/2016/03/16-current-bmj-education-coi-form.pdf.
Provenance and peer review: Commissioned; not peer reviewed.
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Epidemiology and Prevention, Council on the Kidney in Cardiovascular Disease, and
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cardiovascular disease: An update to the scientific statement from the American Heart
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7Maher BA, AhmedIA, Karloukovski V, etal . Magnetite pollution nanoparticles in the human
brain. Proc Natl Acad Sci U S A 2016;113:10797-801.
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vascular disease. ACS Nano 2017;11:4542-52. 10.1021/acsnano.6b08551. 28443337
9 Wei Y, Wang Y, Di Q, etal . Short term exposure to fine particulate matter and hospital
admission risks and costs in the Medicare population: time stratified, case crossover
study. BMJ 2019;367:l6258.
10 Burnett R, Chen H, Szyszkowicz M, etal . Global estimates of mortality associated with
long-term exposure to outdoor fine particulate matter. Proc Natl Acad Sci U S A
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11 Khreis H, Cirach M, Mueller N, etal . Outdoor air pollution and the burden of childhood
asthma across Europe. Eur Respir J 2019;54:1802194.
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13 Di Q, Wang Y, Zanobetti A, etal . Air pollution and mortality in the Medicare opulation. N
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15 Tessum CW, Apte JS, Goodkind AL, etal . Inequity in consumption of goods and services
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EDITORIALS
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... Furthermore, within the genderstratified analysis, PM2.5 exhibited a more significant influence on HDL levels among older men compared to the older women, which may be attributed to the differences in hormone and metabolic levels caused by gender. Numerous previous investigations have explored the deleterious impacts of PM 2.5 on overall health status and psychological well-being [19][20][21]. The extant literature consistently demonstrates a noteworthy association between air pollutants and dyslipidemia. ...
The association between long-term exposure to ambient PM2.5 and high-density lipoprotein cholesterol level among chinese middle-aged and older adults
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Background Recently, the impact of PM2.5 on human health has been intensively studied, especially the respiratory system. High-density lipoprotein plays a crucial role in removing excess cholesterol from cells and transporting it to the liver for excretion. However, the effects of ambient PM2.5 on high-density lipoprotein (HDL) level have not been further studied. Our research aims to investigate the potential association between ambient PM2.5 concentrations and high-density lipoprotein (HDL) levels within the middle-aged and older adults in China. Methods We employed data from individuals aged 45 years and above who were participants in Wave 3 of the China Health and Retirement Longitudinal Study (CHARLS). The high-quality, high-resolution PM2.5 exposure concentration data for each participant were obtained from the ChinaHighAirPollutants (CHAP) dataset, while the HDL levels were derived from blood samples collected during CHARLS Wave 3. This analysis constitutes a cross-sectional study involving a total of 12,519 participants. To investigate associations, we conducted multivariate linear regression analysis, supplemented by subgroup analysis. Results In this cross-sectional investigation, we discerned a negative association between prolonged exposure to ambient PM2.5 constituents and high-density lipoprotein (HDL) levels. The observed correlation between ambient PM2.5 and HDL levels suggests that older individuals residing in areas with elevated PM2.5 concentrations exhibit a reduction in HDL levels (Beta: -0.045; 95% CI: -0.056, -0.035; P < 0.001). Upon adjusting for age in Model I, the Beta coefficient remained consistent at -0.046 (95% CI: -0.056, -0.035; p < 0.001). This association persisted even after accounting for various potential confounding factors (Beta = -0.031, 95% CI: -0.041, -0.021, p < 0.001). Conclusions Our study reveals a statistically significant negative correlation between sustained exposure to higher concentrations of ambient PM2.5 and high-density lipoprotein (HDL) levels among Chinese middle-aged and older individuals.
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... It occurs when harmful gases, particulate matter, and chemicals are released into the air. Long-term exposure to air pollution has also been linked to an increased risk of heart disease, stroke, lung cancer, and premature death [33]. Carla et al. highlighted the connection between air pollutant exposure and excessive body fat, and this finding was further supported by animal experiments [34]. ...
Causal Relationships between Air Pollutant Exposure and Bone Mineral Density and the Risk of Bone Fractures: Evidence from a Two-Stage Mendelian Randomization Analysis
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A number of studies from the literature have suggested that exposure to air pollutants is associated with a declined bone mineral density (BMD), and increased risks of osteoporosis (OP) and bone fractures. This study was performed to systemically assess the genetically causal associations of air pollutants with site-/age-specific BMD and risk of bone fractures with the implementation of two-sample Mendelian randomization (TSMR) and multivariate Mendelian randomization (MVMR). The TSMR analysis was implemented to infer the causal associations between air pollutants and BMD and the risk of bone fractures, additional MVMR analysis was used to further estimate the direct causal effects between air pollutants and BMD, the occurrence of OP, and bone fractures. The results showed that NOx exposure contributed to lower femoral neck BMD (FN-BMD) (β = −0.71, 95%CI: −1.22, −0.20, p = 0.006) and total body BMD (TB-BMD) (β = −0.55, 95%CI: −0.90, −0.21, p = 0.002). Additionally, exposure to PM10 was found to be associated with a decreased TB-BMD (B β = −0.42, 95%CI: −0.66, −0.18, p = 0.001), further age-specific subgroup analysis demonstrated the causal effect of PM10 exposure on the decreased TB-BMD in a subgroup aged 45 to 60 years (β = −0.70, 95%CI: −1.12, −0.29, p = 0.001). Moreover, the findings of the MVMR analysis implied that there was a direct causal effect between PM10 exposure and the decreased TB-BMD (45 < age < 60), after adjusting for PM2.5 and PM2.5 —10 exposure. Our study provides additional evidence to support the causal associations of higher concentrations of air pollutant exposure with decreased BMD, especially in those populations aged between 45 to 60 years, suggesting that early intervention measures and public policy should be considered to improve public health awareness and promote bone health.
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... Recently, the key driving role of air pollution in IHD has attracted an increasing amount of attention in recent years (Künzli et al., 2011;Langrish et al., 2014). Fine particulate matter (particulate matter less than or equal to 2.5 μm in aerodynamic diameter; PM 2.5 ), are able to enter the bloodstream through the lungs and may adversely affect vital organs, such as heart and pancreas (Loxham et al., 2019;Xing et al., 2016). Epidemiological and experimental studies have consistently shown that the incidence and mortality of IHD are linked to PM 2.5 exposure (Lippmann, 2014;Martinelli et al., 2013). ...
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... There are also a large number of PAHs in PM; PM is an air pollution category that comprises both liquid droplets and solid airborne particles, which is a kind of air pollution that has been identified as a human carcinogen (Group I). PM2.5, which is defined as particles and droplets with an aerodynamic diameter of less than 2.5 μm, has been linked to the development and exacerbation of respiratory diseases, such as asthma, pulmonary fibrosis, chronic obstructive pulmonary diseases, and lung cancer (Burney and Amaral 2019;Loxham et al. 2019). China is one of the countries with severe PM2.5 pollution in recent years, particularly in metropolitan areas (Zhang and Cao 2015). ...
The role of N6-methyladenosine methylation in PAHs-induced cancers
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Polycyclic aromatic hydrocarbons (PAHs), which are a wide range of environmental toxicants, may act on humans through inhalation, ingestion, and skin contact, resulting in a range of toxic reactions. Epidemiological studies showed that long-term exposure to PAHs in the occupational and living environment results in a substantial rise in the incidence rate of many cancers in the population, so the prevention and treatment of these diseases have become a major worldwide public health problem. N6-methyladenosine (m6A) modification greatly affects the metabolism of RNA and is implicated in the etiopathogenesis of many kinds of diseases. In addition, m6A-binding proteins have an important role in disease development. The abnormal expression of these can cause the malignant proliferation, migration, invasion, and metastasis of cancers. Furthermore, a growing number of studies revealed that environmental toxicants are one of the cancer risk factors and are related to m6A modifications. Exposure to environmental toxicants can alter the methylation level of m6A and the expression of the m6A-binding protein, thus promoting the occurrence and development of cancers through diverse mechanisms. m6A may serve as a biomarker for early environmental exposure. Through the study of m6A, we can find the health injury early, thus providing a new sight for preventing and curing environmental health-related diseases.
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... Where t is the day of observation; Yt denotes daily count of hospital admissions for CSD at day t; Xt is the daily mean concentration of PM 2.5 at day t; β is the regression coefficient which represents the log-relative rate of hospital admissions for CSD with a 10 µg/m 3 increase of PM 2.5 concentration; DOW means the day of the week; df is degree of freedom whose value is determined based on the Quasi-Akaike information criterion (QAIC); α is the model intercept. It is universally accepted that ambient air pollutants have persistent and hysteresis effects on health outcomes (16). We considered both single-day lags (lag0-lag14) and multiday lags (lag01-lag014) to evaluate delayed effects of PM 2.5 . ...
Associations between short-term PM2.5 exposure and daily hospital admissions for circulatory system diseases in Ganzhou, China: A time series study
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Full-text available
  • Mar 2023
Objective Previous epidemiological studies have shown that both long-term and short-term exposure to fine particulate matters (PM2.5) were associated with the morbidity and mortality of circulatory system diseases (CSD). However, the impact of PM2.5 on CSD remains inconclusive. This study aimed to investigate the associations between PM2.5 and circulatory system diseases in Ganzhou. Methods We conducted this time series study to explore the association between ambient PM2.5 exposure and daily hospital admissions for CSD from 2016 to 2020 in Ganzhou by using generalized additive models (GAMs). Stratified analyses were also performed by gender, age, and season. Results Based on 201,799 hospitalized cases, significant and positive associations were found between short-term PM2.5 exposure and hospital admissions for CSD, including total CSD, hypertension, coronary heart disease (CHD), cerebrovascular disease (CEVD), heart failure (HF), and arrhythmia. Each 10 μg/m³ increase in PM2.5 concentrations was associated with a 2.588% (95% confidence interval [CI], 1.161%–4.035%), 2.773% (95% CI, 1.246%–4.324%), 2.865% (95% CI, 0.786%–4.893%), 1.691% (95% CI, 0.239%–3.165%), 4.173% (95% CI, 1.988%–6.404%) and 1.496% (95% CI, 0.030%–2.983%) increment in hospitalizations for total CSD, hypertension, CHD, CEVD, HF, and arrhythmia, respectively. As PM2.5 concentrations rise, the hospitalizations for arrhythmia showed a slow upward trend, while other CSD increased sharply at high PM2.5 levels. In subgroup analyses, the impacts of PM2.5 on hospitalizations for CSD were not materially changed, although the females had higher risks of hypertension, HF, and arrhythmia. The relationships between PM2.5 exposure and hospitalizations for CSD were more significant among individuals aged ≤65 years, except for arrhythmia. PM2.5 had stronger effects on total CSD, hypertension, CEVD, HF, and arrhythmia during cold seasons. Conclusion PM2.5 exposure was positively associated with daily hospital admissions for CSD, which might provide informative insight on adverse effects of PM2.5.
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Nutrient synergy refers to the concept that the combined effects of two or more nutrients working together have a greater physiological impact on the body than when each nutrient is consumed individually. While nutrition science traditionally focuses on isolating single nutrients to study their effects, it is recognized that nutrients interact in complex ways, and their combined consumption can lead to additive effects. Additionally, the Dietary Reference Intakes (DRIs) provide guidelines to prevent nutrient deficiencies and excessive intake but are not designed to assess the potential synergistic effects of consuming nutrients together. Even the term synergy is often applied in different manners depending on the scientific discipline. Considering these issues, the aim of this narrative review is to investigate the potential health benefits of consuming different nutrients and nutrient supplements in combination, a concept we define as nutrient synergy, which has gained considerable attention for its impact on overall well-being. We will examine how nutrient synergy affects major bodily systems, influencing systemic health. Additionally, we will address the challenges associated with promoting and conducting research on this topic, while proposing potential solutions to enhance the quality and quantity of scientific literature on nutrient synergy.
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Effect of Meteorological Factors, Air Pollutants on Daily Hospital Admissions for Ischemic Heart Disease in Lanzhou, China
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  • Jul 2023
  • CARDIOLOGY
Background: Meteorological factors and air pollutants are believed to be associated with cardiovascular disease. Ischemic heart disease (IHD) is a major public health issue worldwide. Few studies have investigated the associations among meteorological factors, air pollutants and IHD daily hospital admissions in Lanzhou, China. Methods: We conducted a distributed lag non-linear model (DLNM) on the basis of five years data, aiming at disentangling the impact of meteorological factors and air pollutants on IHD hospital admissions. All IHD daily hospital admissions recorded from January 1, 2015 and December 31, 2019 were obtained from three hospitals in Lanzhou, China. Daily air pollutant concentrations and meteorological data were synchronously collected from Gansu Meteorological Administration and Lanzhou Environmental Protection Administration. Stratified analyses were performed by sex and two age-groups. Results: A total of 23555 IHD hospital admissions were recorded, of which 10477 admissions were for coronary artery disease (CAD), 13078 admissions were for acute coronary syndrome (ACS). Our results showed that there was a non-linear (J-shaped) relationship between temperature and IHD hospital admissions. The number of IHD hospital admissions were positively correlated with NO2, O3, humidity and pressure, indicating an increased risk of hospital admissions for IHD under NO2, O3, humidity and pressure exposure. Meanwhile, both extremely low (-12ºC) and high (30ºC) temperature reduced IHD hospital admissions, but the harmful effect increased with the lag time in Lanzhou, China, while the cold effect was more pronounced and long-lasting than the heat effect. Subgroup analysis demonstrated that the risk on CAD hospital admissions increased significantly in female and <65 years of age at -12ºC. Conclusion: Our findings added to the growing evidence regarding the potential impact of meteorological factors, air pollutants on policymaking from the perspective of hospital management efficiency.
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Electroactive, Antibacterial, and Biodegradable Poly(lactic acid) Nanofibrous Air Filters for Healthcare
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  • Jun 2023
  • ACS APPL MATER INTER
Poly(lactic acid) (PLA)-based nanofibrous membranes (NFMs) hold great potential in the field of biodegradable filters for air purification but are largely limited by the relatively low electret properties and high susceptibility to bacteria. Herein, we disclosed a facile approach to the fabrication of electroactive and antibacterial PLA NFMs impregnated with a highly dielectric photocatalyst. In particular, the microwave-assisted doping (MAD) protocol was employed to yield Zn-doped titanium dioxide (Zn-TIO), featuring the well-defined anatase phase, a uniform size of ∼65 nm, and decreased band gap (3.0 eV). The incorporation of Zn-TIO (2, 6, and 10 wt %) into PLA gave rise to a significant refinement of the electrospun nanofibers, decreasing from the highest diameter of 581 nm for pure PLA to the lowest value of 264 nm. More importantly, dramatical improvements in the dielectric constants, surface potential, and electret properties were simultaneously achieved for the composite NFMs, as exemplified by a nearly 94% increase in surface potential for 3-day-aged PLA/Zn-TIO (90/10) compared with that of pure PLA. The well regulation of morphological features and promotion of electroactivity contributed to a distinct increase in the air filtration performance, as demonstrated by 98.7% filtration of PM0.3 with the highest quality factor of 0.032 Pa-1 at the airflow velocity of 32 L/min for PLA/Zn-TIO (94/6), largely surpassing pure PLA (89.4%, 0.011 Pa-1). Benefiting from the effective generation of reactive radicals and gradual release of Zn2+ by Zn-TIO, the electroactive PLA NFMs were ready to profoundly inactivate Escherichia coli and Staphylococcus epidermidis. The exceptional combination of remarkable electret properties and excellent antibacterial performance makes the PLA membrane filters promising for healthcare.
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Toxicological Profile of PM from Different Sources in the Bronchial Epithelial Cell Line BEAS-2B
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Full-text available
  • Apr 2023
The toxicity of particulate matter (PM) is strictly associated with its physical-chemical characteristics, such as size or chemical composition. While these properties depend on the origin of the particles, the study of the toxicological profile of PM from single sources has rarely been highlighted. Hence, the focus of this research was to investigate the biological effects of PM from five relevant sources of atmospheric PM: diesel exhaust particles, coke dust, pellet ashes, incinerator ashes, and brake dust. Cytotoxicity, genotoxicity, oxidative, and inflammatory response were assessed in a bronchial cell line (BEAS-2B). BEAS-2B cells were exposed to different concentrations (25, 50, 100, and 150 μg/mL medium) of particles suspended in water. The exposure lasted 24 h for all the assays performed, except for reactive oxygen species, which were evaluated after 30 min, 1 h, and 4 h of treatment. The results showed a different action of the five types of PM. All the tested samples showed a genotoxic action on BEAS-2B, even in the absence of oxidative stress induction. Pellet ashes seemed to be the only ones able to induce oxidative stress by boosting the formation of reactive oxygen species, while brake dust resulted in the most cytotoxic. In conclusion, the study elucidated the differential response of bronchial cells to PM samples generated by different sources. The comparison could be a starting point for a regulatory intervention since it highlighted the toxic potential of each type of PM tested.
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Short term exposure to fine particulate matter and hospital admission risks and costs in the Medicare population: Time stratified, case crossover study
Article
Full-text available
  • Nov 2019
Objective To assess risks and costs of hospital admission associated with short term exposure to fine particulate matter with diameter less than 2.5 µm (PM 2.5 ) for 214 mutually exclusive disease groups. Design Time stratified, case crossover analyses with conditional logistic regressions adjusted for non-linear confounding effects of meteorological variables. Setting Medicare inpatient hospital claims in the United States, 2000-12 (n=95 277 169). Participants All Medicare fee-for-service beneficiaries aged 65 or older admitted to hospital. Main outcome measures Risk of hospital admission, number of admissions, days in hospital, inpatient and post-acute care costs, and value of statistical life (that is, the economic value used to measure the cost of avoiding a death) due to the lives lost at discharge for 214 disease groups. Results Positive associations between short term exposure to PM 2.5 and risk of hospital admission were found for several prevalent but rarely studied diseases, such as septicemia, fluid and electrolyte disorders, and acute and unspecified renal failure. Positive associations were also found between risk of hospital admission and cardiovascular and respiratory diseases, Parkinson’s disease, diabetes, phlebitis, thrombophlebitis, and thromboembolism, confirming previously published results. These associations remained consistent when restricted to days with a daily PM 2.5 concentration below the WHO air quality guideline for the 24 hour average exposure to PM 2.5 . For the rarely studied diseases, each 1 µg/m ³ increase in short term PM 2.5 was associated with an annual increase of 2050 hospital admissions (95% confidence interval 1914 to 2187 admissions), 12 216 days in hospital (11 358 to 13 075), US$31m (£24m, €28m; $29m to $34m) in inpatient and post-acute care costs, and $2.5bn ($2.0bn to $2.9bn) in value of statistical life. For diseases with a previously known association, each 1 µg/m ³ increase in short term exposure to PM 2.5 was associated with an annual increase of 3642 hospital admissions (3434 to 3851), 20 098 days in hospital (18 950 to 21 247), $69m ($65m to $73m) in inpatient and post-acute care costs, and $4.1bn ($3.5bn to $4.7bn) in value of statistical life. Conclusions New causes and previously identified causes of hospital admission associated with short term exposure to PM 2.5 were found. These associations remained even at a daily PM 2.5 concentration below the WHO 24 hour guideline. Substantial economic costs were linked to a small increase in short term PM 2.5 .
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Cardiovascular disease burden from ambient air pollution in Europe reassessed using novel hazard ratio functions
Article
Full-text available
  • May 2019
  • EUR HEART J
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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Inequity in consumption of goods and services adds to racial–ethnic disparities in air pollution exposure
Article
Full-text available
  • Mar 2019
Fine particulate matter (PM 2.5 ) air pollution exposure is the largest environmental health risk factor in the United States. Here, we link PM 2.5 exposure to the human activities responsible for PM 2.5 pollution. We use these results to explore “pollution inequity”: the difference between the environmental health damage caused by a racial–ethnic group and the damage that group experiences. We show that, in the United States, PM 2.5 exposure is disproportionately caused by consumption of goods and services mainly by the non-Hispanic white majority, but disproportionately inhaled by black and Hispanic minorities. On average, non-Hispanic whites experience a “pollution advantage”: They experience ∼17% less air pollution exposure than is caused by their consumption. Blacks and Hispanics on average bear a “pollution burden” of 56% and 63% excess exposure, respectively, relative to the exposure caused by their consumption. The total disparity is caused as much by how much people consume as by how much pollution they breathe. Differences in the types of goods and services consumed by each group are less important. PM 2.5 exposures declined ∼50% during 2002–2015 for all three racial–ethnic groups, but pollution inequity has remained high.
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Global estimates of mortality associated with long-term exposure to outdoor fine particulate matter
Article
Full-text available
  • Sep 2018
Exposure to ambient fine particulate matter (PM2.5) is a major global health concern. Quantitative estimates of attributable mortality are based on disease-specific hazard ratio models that incorporate risk information from multiple PM2.5 sources (outdoor and indoor air pollution from use of solid fuels and secondhand and active smoking), requiring assumptions about equivalent exposure and toxicity. We relax these contentious assumptions by constructing a PM2.5-mortality hazard ratio function based only on cohort studies of outdoor air pollution that covers the global exposure range. We modeled the shape of the association between PM2.5 and nonaccidental mortality using data from 41 cohorts from 16 countries-the Global Exposure Mortality Model (GEMM). We then constructed GEMMs for five specific causes of death examined by the global burden of disease (GBD). The GEMM predicts 8.9 million [95% confidence interval (CI): 7.5-10.3] deaths in 2015, a figure 30% larger than that predicted by the sum of deaths among the five specific causes (6.9; 95% CI: 4.9-8.5) and 120% larger than the risk function used in the GBD (4.0; 95% CI: 3.3-4.8). Differences between the GEMM and GBD risk functions are larger for a 20% reduction in concentrations, with the GEMM predicting 220% higher excess deaths. These results suggest that PM2.5 exposure may be related to additional causes of death than the five considered by the GBD and that incorporation of risk information from other, nonoutdoor, particle sources leads to underestimation of disease burden, especially at higher concentrations.
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Air Pollution and Mortality in the Medicare Population
Article
Full-text available
  • Jun 2017
Background Studies have shown that long-term exposure to air pollution increases mortality. However, evidence is limited for air-pollution levels below the most recent National Ambient Air Quality Standards. Previous studies involved predominantly urban populations and did not have the statistical power to estimate the health effects in underrepresented groups. Methods We constructed an open cohort of all Medicare beneficiaries (60,925,443 persons) in the continental United States from the years 2000 through 2012, with 460,310,521 person-years of follow-up. Annual averages of fine particulate matter (particles with a mass median aerodynamic diameter of less than 2.5 μm [PM2.5]) and ozone were estimated according to the ZIP Code of residence for each enrollee with the use of previously validated prediction models. We estimated the risk of death associated with exposure to increases of 10 μg per cubic meter for PM2.5 and 10 parts per billion (ppb) for ozone using a two-pollutant Cox proportional-hazards model that controlled for demographic characteristics, Medicaid eligibility, and area-level covariates. Results Increases of 10 μg per cubic meter in PM2.5 and of 10 ppb in ozone were associated with increases in all-cause mortality of 7.3% (95% confidence interval [CI], 7.1 to 7.5) and 1.1% (95% CI, 1.0 to 1.2), respectively. When the analysis was restricted to person-years with exposure to PM2.5 of less than 12 μg per cubic meter and ozone of less than 50 ppb, the same increases in PM2.5 and ozone were associated with increases in the risk of death of 13.6% (95% CI, 13.1 to 14.1) and 1.0% (95% CI, 0.9 to 1.1), respectively. For PM2.5, the risk of death among men, blacks, and people with Medicaid eligibility was higher than that in the rest of the population. Conclusions In the entire Medicare population, there was significant evidence of adverse effects related to exposure to PM2.5 and ozone at concentrations below current national standards. This effect was most pronounced among self-identified racial minorities and people with low income. (Supported by the Health Effects Institute and others.)
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A joint ERS/ATS policy statement: what constitutes an adverse health effect of air pollution? An analytical framework
Article
Full-text available
  • Dec 2016
The American Thoracic Society has previously published statements on what constitutes an adverse effect on health of air pollution in 1985 and 2000. We set out to update and broaden these past statements that focused primarily on effects on the respiratory system. Since then, many studies have documented effects of air pollution on other organ systems, such as on the cardiovascular and central nervous systems. In addition, many new biomarkers of effects have been developed and applied in air pollution studies. This current report seeks to integrate the latest science into a general framework for interpreting the adversity of the human health effects of air pollution. Rather than trying to provide a catalogue of what is and what is not an adverse effect of air pollution, we propose a set of considerations that can be applied in forming judgments of the adversity of not only currently documented, but also emerging and future effects of air pollution on human health. These considerations are illustrated by the inclusion of examples for different types of health effects of air pollution. Air pollution has many effects on health; this document provides guidance to judge the adversity of such effects
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Outdoor Air Pollution and the Burden of Childhood Asthma across Europe
Article
  • Aug 2019
Background Emerging evidence suggests that air pollution may contribute to childhood asthma development. We estimated the burden of incident childhood asthma that may be attributable to outdoor NO 2 , PM 2.5 and black carbon (BC) in Europe. Methods We combined country-level childhood incidence rates and pooled exposure-response functions with children's (1–14 years) counts, and exposure estimates at 1 540 386 1 km×1 km cells, across 18 European countries and 63 442 419 children. Annual average pollutant concentrations were obtained from a validated and harmonised European land-use regression (LUR) model. We investigated two exposure reduction scenarios. For the first, we used recommended annual World Health Organization (WHO) air quality guideline values. For the second, we used the minimum air pollution levels recorded across 41 studies in the underlying meta-analysis. Results NO 2 ranged from 1.4 to 70.0 µg·m ⁻³ , with a mean of 11.8 µg·m ⁻³ . PM 2.5 ranged from 2.0 to 41.1 µg·m ⁻³ , with a mean of 11.6 µg·m ⁻³ . BC ranged from 0.003 to 3.7×10 ⁻⁵ m ⁻¹ , with a mean of 1.0×10 ⁻⁵ m ⁻¹ . Compliance with the NO 2 and PM 2.5 WHO guidelines, respectively, was estimated to prevent 2434 (0.4%) and 66 567 (11%) incident cases. Meeting the minimum air pollution levels for NO 2 (1.5 µg·m ⁻³ ), PM 2.5 (0.4 µg·m ⁻³ ) and BC (0.4×10 ⁻⁵ m ⁻¹ ), respectively, was estimated to prevent 135 257 (23%), 191 883 (33%) and 89 191 (15%) incident cases. Conclusions A significant proportion of childhood asthma cases may be attributable to outdoor air pollution, and these cases could be prevented. Our estimates underline an urgent need to reduce children's exposure to air pollution.
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Air Pollution and Noncommunicable Diseases: A Review by the Forum of International Respiratory Societies’ Environmental Committee, Part 2: Air Pollution and Organ Systems
Article
  • Nov 2018
Although air pollution is well-known to be harmful to the lung and airways, it can also damage most other organ systems of the body. It is estimated that about 500,000 lung cancer deaths and 1.6 million chronic obstructive pulmonary disease (COPD) deaths can be attributed to air pollution, but air pollution may also account for 19% of all cardiovascular deaths and 21% of all stroke deaths. Air pollution has been linked to other malignancies, such as bladder cancer and childhood leukemia. Lung development in childhood is stymied with exposure to air pollutants, and poor lung development in children predicts lung impairment in adults. Air pollution is associated with reduced cognitive function and increased risk of dementia. Particulate matter in the air (PM2.5) is associated with delayed psychomotor development and lower child intelligence. Studies link air pollution with diabetes mellitus prevalence, morbidity, and mortality. Pollution affects the immune system and is associated with allergic rhinitis, allergic sensitization, and autoimmunity. It is also associated with osteoporosis and bone fractures, conjunctivitis, dry eye disease, and blepharitis, inflammatory bowel disease, increased intravascular coagulation, and decreased glomerular filtration rate. Atopic and urticarial skin disease, acne, and skin aging are linked to air pollution. Air pollution is controllable and, therefore, many of these adverse health effects can be prevented.
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Inhaled Nanoparticles Accumulate at Sites of Vascular Disease
Article
  • Apr 2017
The development of engineered nanomaterials is growing exponentially, despite concerns over their potential similarities to environmental nanoparticles that are associated with significant cardiorespiratory morbidity and mortality. The mechanisms through which inhalation of nanoparticles could trigger acute cardiovascular events are emerging, but a fundamental unanswered question remains: Do inhaled nanoparticles translocate from the lung in man and directly contribute to the pathogenesis of cardiovascular disease? In complementary clinical and experimental studies, we used gold nanoparticles to evaluate particle translocation, permitting detection by high-resolution inductively coupled mass spectrometry and Raman microscopy. Healthy volunteers were exposed to nanoparticles by acute inhalation, followed by repeated sampling of blood and urine. Gold was detected in the blood and urine within 15 min to 24 h after exposure, and was still present 3 months after exposure. Levels were greater following inhalation of 5 nm (primary diameter) particles compared to 30 nm particles. Studies in mice demonstrated the accumulation in the blood and liver following pulmonary exposure to a broader size range of gold nanoparticles (2-200 nm primary diameter), with translocation markedly greater for particles <10 nm diameter. Gold nanoparticles preferentially accumulated in inflammation-rich vascular lesions of fat-fed apolipoproteinE-deficient mice. Furthermore, following inhalation, gold particles could be detected in surgical specimens of carotid artery disease from patients at risk of stroke. Translocation of inhaled nanoparticles into the systemic circulation and accumulation at sites of vascular inflammation provides a direct mechanism that can explain the link between environmental nanoparticles and cardiovascular disease and has major implications for risk management in the use of engineered nanomaterials.
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Transboundary health impacts of transported global air pollution and international trade
Article
  • Mar 2017
  • NATURE
Millions of people die every year from diseases caused by exposure to outdoor air pollution. Some studies have estimated premature mortality related to local sources of air pollution but local air quality can also be affected by atmospheric transport of pollution from distant sources. International trade is contributing to the globalization of emission and pollution as a result of the production of goods (and their associated emissions) in one region for consumption in another region. The effects of international trade on air pollutant emissions, air quality and health have been investigated regionally, but a combined, global assessment of the health impacts related to international trade and the transport of atmospheric air pollution is lacking. Here we combine four global models to estimate premature mortality caused by fine particulate matter (PM_(2.5)) pollution as a result of atmospheric transport and the production and consumption of goods and services in different world regions. We find that, of the 3.45 million premature deaths related to PM_(2.5) pollution in 2007 worldwide, about 12 per cent (411,100 deaths) were related to air pollutants emitted in a region of the world other than that in which the death occurred, and about 22 per cent (762,400 deaths) were associated with goods and services produced in one region for consumption in another. For example, PM_(2.5) pollution produced in China in 2007 is linked to more than 64,800 premature deaths in regions other than China, including more than 3,100 premature deaths in western Europe and the USA; on the other hand, consumption in western Europe and the USA is linked to more than 108,600 premature deaths in China. Our results reveal that the transboundary health impacts of PM_(2.5) pollution associated with international trade are greater than those associated with long-distance atmospheric pollutant transport.
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