Effect of Particulate Matter On Human Health, Prevention, and Imaging Using Pet or Spect
Effect of Particulate Matter On Human Health, Prevention, and Imaging Using Pet or Spect
Effect of Particulate Matter On Human Health, Prevention, and Imaging Using Pet or Spect
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Progress in Medical Physics 29(3), September 2018
Review Article https://doi.org/10.14316/pmp.2018.29.3.81
eISSN 2508-4453
Received 1 September 2018 Particulate matter (PM) in dust causes serious pathological conditions, and it has been considered a
Revised 11 September 2018 critical health issue for many years. Respiratory disorders such as bronchitis, asthma, and chronic
Accepted 11 September 2018 inflammation, are the most common illnesses due to PM that appears as dust. There is evidence
that cardiovascular and neurological abnormalities are caused by PM. Although an extensive
Corresponding author amount of work has been conducted on this topic, including studies on the nature of the particles,
Jin Su Kim particle size measurements, particle distribution upon inhalation, the health effects of fine particles,
([email protected]) disease prevention, diagnosis, and treatment, to this date, there is still a considerable lack of
Tel: 82-2-970-1661 knowledge in these areas. Therefore, the identification of the key components that cause diseases
Fax: 82-2-970-1341 owing to PM, and the specific diagnoses of the diseases, is important. This review will explore the
current literature on the origin and nature of PM and their effects on human health. In addition, it
will also highlight the approaches that have been adopted in order to diagnose the effects of PM
using positron emission tomography (PET) or single-photon emission computerized tomography
(SPECT).
to be sulfate (20%), crustal material (13.4%), equivalent G et al. thus, revealing data on variation in the global PM
black carbon (11.9%), ammonium nitrate (4.7%), sea salt chemical composition.5)
(2.3%), trace metal oxides (1.0%), water (7.2%) at 35% rela-
tive humidity, and residual matter (40%).5) In a study con- Particulate Matter and Its
ducted in 2005, the inspection of the Saharan desert dust Impact on Human Health
was carried out using scanning electron microscopy.6) The
mineralogical phase composition by transmission electron Pollutants from many different sources were parts of the
microscopy and aerosol size distribution by optical particle air we inhale. The type of pollutant varied depending on
spectrometer were studied and compared. Results revealed the geographical distribution, area, workplace, and sea-
that the average composition (by volume) of aerosol was son. Personnel working in industrial areas was more prone
dominated by mineral dust contained 64% silicates, 6% to air pollution. The PM derived from various pollution
quartz, 5% calcium-rich particles, 14% sulfates, 1% hema- sources upon inhalation produces serious effects on the
tite, 1% soot, and 9% of other carbonaceous materials es- skin, arteries, lungs, heart, and eyes.12-19) The brain was also
pecially for particles larger than 1 μm.6) affected by the PM, depending upon the particulate size
The composition of PM in Asia investigated by the Asian and charge.20) The characteristics of the PM determined
Pacific Regional Characterization Experiment (ACE/Asia) the potential biological effects.21) A group of researchers
revealed that the primary components of fine particles in showed that the size of PM regulated its potential to cause
2+ 2+ 7)
mixed mineral dust-pollution plumes were Mg and Ca . an injury, or oxidative, inflammatory, and other biological
Moreover, the composition of roadside dust was domi- responses.1,21)
nated by Fe, Cr, and Ni, while particles rich in W and trace Both long- and short-time exposures to PM was of seri-
elements were also reported, as suggested by a study in ous concern. Sustained long-time exposure in the environ-
4)
Finland using scanning electron microscopy. In modern ment for many years was linked to serious cardiovascular,
concrete jungles, the concentration of PM was greatly in- respiratory, and skin diseases. Short-time exposure led to
creased, and its adverse effects on humans were propelled morbidity incidents in all ages owing to cardiovascular and
the utter need to design strategies for diagnosis and pre- respiratory diseases caused by inhalation of airborne dust
vention. Demolition of buildings and concrete structures particles.22) According to the United Nations environmental
were considered as one of the major sources of aerosol program, approximately 1.1 billion people died owing to
dust emission.7,8) A study was conducted in Baltimore (USA) PM. Inhaled PM can penetrate deeply into the lungs, which
which suggested a great increase in PM after experimenta- constituted a particular concern owing to the serious
8,9)
tion on three demolition sites. In another study in Tokyo, hazardous effects they cause. There was an evidence that
PM samples were collected from streets, and hydrocarbons airborne particles was associated with cardiovascular dis-
were analyzed using capillary gas chromatography fol- eases.23) There was a report that PM was a possible cause of
lowing HPLC fractionation. The study suggested that PM stroke.24)
in metropolitan cities was mainly owing to automobile Table 1 listed the classification and related pronounced
exhausts and the burning of fuels, while residential areas pathological conditions documented thus far. Fig. 1 shows
receive significant amounts of dust from the settling of PM the diagrammatic representation of inhaled PM of variable
10)
emitted from forest fires, volcanic eruptions, etc.. Indus- sizes and imaging of effect of PM on human health using
tries served as major contributors to the particulate mat- Positron Emission Tomography (PET) or Single-Photon
11,12)
ters by releasing gases that contain particles. Moreover Emission Computerized Tomography (SPECT).
in a long term project of surface particulate matter network
(SPARTAN) various ions, and trace metals were charac- Effects of Particulate Matter on Heart
terized and quantified from worldwide data collection.
Details of the contents can be found in the paper by Snider Air pollution and its associated cardiac risk, as published
www.ksmp.or.kr
Progress in Medical Physics Vol. 29, No. 3, September 2018 83
Brain
Inhaled PM
Imaging Ischemic stroke
PET/SPECT Neuro-inflammation
<0.1 m Cognitive deficit
10 m
2.5 m
Lungs
Heart
Fig. 1. Diagrammatic representation
Cystic fibrosis of inhaled particulate matter (PM) of
Asthma variable sizes. PM-linked respiratory,
Chronic inflammation Myocardial infraction cardiovascular, and neurological dis
Ischemic heart orders and imaging of effect of PM on
disease human health using PET or SPECT.
by the American Heart Association, underlines the set aim to term exposure to PM was fewer, and involved the total
investigate the harmful cardiovascular effects that arise from mortality as well as cardiovascular events. Increased alveo-
the exposure to air pollution. Many researchers reported lar inflammation occurred as a result of the inhaled par-
that particles with diameters of 2.5 μm or less was associated ticles that further exacerbate any preexisting lung disease,
with the elevated risks of cardiovascular events.23,25) Cardio- thus causing increased blood coagulation, and ultimately
vascular risk implications that could arise from the changes leading to increased cardiac risk factors.28,29) Middleton et
in the blood composition include the irregularity of the al, analyzed the respiratory and cardiovascular morbidity
heart rate, and plasma viscosity and blood pressure changes. of short-term exposure of air pollution and dust storms in
In addition, increases in PM concentrations was associated two hospitals in Nicosia, Cyprus. They reported an increase
23,25)
with increased chances for myocardial infarction. in hospital admissions for cardiovascular events by 1.2%
Epidemiological research was initiated after the in- for every elevation in particle concentration by 10 μg/m3
creased mortality rates that occurred as a result of the fog (PM10). Moreover, they concluded that risk of cardiovascu-
in the Meuse valley in December 1930, and following the lar disease increased during dust storm days.30) Similarly,
London smog incident of 1952.26,27) Studies on the long- Pope IC et al. reported statistical analyses of long-term
www.ksmp.or.kr
84 Javeria Zaheer, et al:Imaging the Effect of Particulate Matter
exposure of PM increased the chance of ischemia, heart manufacturing of abrasive soap. Similarly, inhalation of as-
failure, and cardiac arrest. A mortality risk in the range of bestos causes asbestosis. Both silicosis and asbestosis were
31)
8% to 18% was linked to increases of PM10. Cardiovascu- incurable and even after exposure ceases, the disease may
lar health effects was correlated between carbon content still progress.43) The changes of lung function was due to a
and the change in blood pressure measurements. Follow- generalized diffuse fibrosis rather than the nodular fibrosis
ing 2 hr exposure to PM, changes in blood pressure were pattern observed in silicosis. The suggested underlining
32,33)
observed. Similarly, a case cross-over study of exposure mechanism was based on the fact that asbestos decompos-
to urban traffic studied the occurrence of myocardial in- es in the lung by depositing SiO2 following the removal of
farction and concluded that the risk of occurrence of this metallic oxides of asbestos.44) Bhattacharjee et al, reviewed
disease may increase in susceptible persons with transient the genetic and epigenetic alteration in occupational expo-
34)
exposure to urban traffic. sure to silicon asbestos and arsenic.45) Asthma, a breathing
In a stratified case cross-over study design, correlation disorder was connected to PM. It was reported that endo-
between cardiovascular disease (CVD) and PM effects toxin, a pro-inflammatory agent present in house dust, may
29,35)
were found from a database in Wales and England. In be the cause of asthma. It was demonstrated by a cross-
summary, the morbidity events in reported publications sectional study design on 69 patients who had rhinitis or
associated with PM include myocardial infarction, stroke, asthma that the concentration of endotoxin in house dust
venous thrombosis, initiation of atherosclerosis, dysfunc- is a contributing factor in the etiology of asthma.46) More-
tion of the autonomic nervous system, ischemic reposition, over, chronic obstructive pulmonary disease (COPD) was
36,37)
and altered ion-channel function in myocardial cells. also associated with PM. Study and research was suggested
that upon exposure to PM10, PM enhanced the chances of
Effect of Particulate Matter on Lungs being affected by COPD. It also affected the functioning of
lungs in elderly and susceptible patients, as explained by
The direct effects of PM may be attributed to the con- Ming-tai Lin et al, in their investigation to identify the asso-
tact of PM on the epithelium of human lung airways. It ciation between acute exacerbation of chronic obstructive
was speculated to be the cause of the toxic effect of PM pulmonary disease and climatic change.47) Another respi-
originated from various chemical sources. These sources ratory disorder was tuberculosis which constitutes a global
included the combustion of fossil fuel, power generation, challenge. A cross-sectional study conducted on slate pen-
vehicle exhaust, industrial process acid, as well as by vari- cil workers and quartz stone crushers who were highly ex-
ous organic compounds, including pathogens, fungi, pol- posed to silica dust showed that the tendency of being af-
38)
lens, and viruses. Using 10-year data from Taiwan’s na- fected by tuberculosis was greater compared to people who
tional health insurance research database (NHIRD), Kang lived in clean environments.48) Bronchitis, the inflamma-
et al, conducted a study on the relationship of the Asian tion of the bronchial tubes was another malady connected
dust storm and number of pneumonia admissions in a Tai- to dust. The PM have been found to cause inflammation of
wan city. The results showed that there was an increased the airway that causes bronchitis. It was more commonly
number of admissions to hospitals during the dust storm found in people exposed to PM, such as in dryland farming
season.39-42) The effects of PM on the lungs was evident be- areas.49)
cause the lungs was the first systemic organ to interact with
PM via the respiratory system upon inhalation. The PM Effect of Particulate Matter on Brain
was cause of numerous diseases, one of which was known
as silicosis, manifested by lung fibrosis caused by the inha- Although the blood brain barrier effectively protects the
lation of dust-containing silica. It was reported that it was brain, this may not always be the case. Thus, this secure
more dominant in humans working in the industries of barrier may not be safe and does not entirely protect the
sandblasting, flint crushing, the ganister industry, and the brain from PM. It was evident that pollution directly af-
www.ksmp.or.kr
Progress in Medical Physics Vol. 29, No. 3, September 2018 85
fects human health in accordance to recent studies that damages localized to the prefrontal cortex.51-53)
have found and reported various toxic effects, including Because the majority of the world population resides in
cardiovascular, respiratory, and neurological toxicities. urban areas, and was prone to PM, the problem of the in-
PM2.5 can cross the blood brain barrier. The effects of PM crease prevalence of CNS diseases would be important and
sizes on the brain were first reported in 1998 by conduct- needs to be investigated. Increases in stroke hospitaliza-
ing a cohort study that comprised 957 patients exposed to tions were observed with PM as Yang et al and Kang et al,
indoor coal fumes in Shanghai. The study indicated that described while working in Taiwan.54,55) Table 2 listed the
the individuals who were exposed to coal fumes yielded studies that were conducted to evaluate the effects of PM
an increase incidence in ischemic stroke that is the lead- on vital organs.
50,51)
ing cause of death in the Shanghai. Recent studies
indicated that PM could attack the brain parenchyma Imaging of the Effects of Particulate Matter
causing neurodegenerative disease. Alzheimer’s disease
(AD) and Parkinson’s disease (PD) are neurodegenera- After inhalation of PM, assessment of their bio distribu-
tive diseases and affect a significant number of humans all tion would be important in terms of risk management.
over the world. To identify the correlation between PM and Many factors was responsible for the PM deposition and
neurodegenerative disease, a prior study was carried out diffusion in the body after inhalation. Nevertheless, limited
on canine naturally exposed to PM. The study concluded data was available on the clinical diagnostic strategy of PM.
that a significant increase in DNA damage (apurinic/apy- Imaging the effects of PM could be conducted using planar
rimidinic sites) in olfactory bulbs, frontal cortex, and hip- scintigraphy, SPECT and PET.
pocampus, were observed when dogs were exposed to PM.
According to the study, the nasal pathways was known the 1. Gamma scintigraphy or SPECT
point of entry for PM. Another study performed on human
and animal models suggested that brain exposed to PM Gamma scintigraphy was a conventional method used
led to increases in CD-68, CD-163, and HLA-DR positive in nuclear medicine for diagnostic purposes.56) The limi-
cells. Also noted, there were elevated pro-inflammatory tation of gamma scintigraphy was the 2D image, and the
markers interleukin-1b, cyclooxygenase 2, increased Ab42 measurement of the distribution of aerosol deposition was
deposition (hallmark disease protein of Alzheimer’s dis- limited owing to the lack of spatial resolution. Laube et al.,
ease), BBB damage, endothelial cell activation, and brain used gamma scintigraphy to measure the targeted aero-
lesions in the prefrontal lobe. Furthermore, these studies solized medication in peripheral airways in cystic fibrosis
suggested that PM caused cytokine production, increases patients, and found that PM deposition can be achieved
in MAP kinase, neurochemical changes, lipid peroxidation, by varying the particle size and inspiratory flow rate.57) To
enhanced NF-kb expression, and behavioral changes. Ex- determine the particle deposition and clearance, the imag-
posure to PM not only causes neuro-inflammation but also ing of radio-aerosoles with gamma cameras was a well-es-
the accumulation of beta amyloids which was considered tablished technique. SPECT imaging was based on the use
to be the cause of AD. Additionally, it leads to increases in of gamma cameras to provide three-dimensional images.
α-synclines which are the components of Lewis bodies, The radioisotopes used with tracer in SPECT imaging are
123
and which was speculated to cause PD. It was found that I, 99mTc, 133Xe, 201Tl, 67Ga and 18F. Whereas among radioiso-
their accumulation starts in childhood when the body was topes, 99mTc was most commonly used tracer.58) Inhaled PM
99m
exposed to PM. Eventually, this causes premature aging in could be traced using Tc-labelled PM. Nemmar et al.’s
the brain, and initiates the development of disease as a re- study showed that 99mTc-labelled particles were deposited
sult of the alteration of the aggregation and rate of protein in the body organ and thus detected over thyroid, salivary
fibrillation by nanoparticles. MRI analyses of brain images glands, liver, bladder and stomach.59)
acquired from children exposed to PM revealed structural
www.ksmp.or.kr
86 Javeria Zaheer, et al:Imaging the Effect of Particulate Matter
Table 2. List of prior conducted studies explaining the effects of PM on systemic organs.
Year Title Reference
Cardiovascular
2018 The association between exposure to air pollutants including PM10, PM2.5, ozone, Akbarzadeh et al.73)
carbon monoxide, sulfur dioxide, and nitrogen dioxide concentrations, and the relative
risk of developing STEMI: A case-crossover design
2014 A 10-year time-series analysis of respiratory and cardiovascular morbidity in Nicosia, Middleton et al.30)
Cyprus: the effects of short-term changes in air pollution and dust storms
2012 Effect of dust storm events on daily emergency admissions for cardiovascular diseases Tam et al.37)
2008 Short-term effects of air pollution on a range of cardiovascular events in England and Milojevic et al.29)
Wales: case-crossover analysis of the MINAP database, hospital admissions, and
mortality
2005 Acute blood pressure responses in healthy adults during controlled air pollution Urch et al.32)
exposures. Environmental health perspectives
2004 Exposure to traffic and the onset of myocardial infarction Peters et al.34)
2003 Air pollution and hospital admissions for ischemic heart diseases among individuals Lee et al.36)
who are 64+ years of age residing in Seoul, Korea
2002 Inhalation of fine particulate air pollution and ozone causes acute arterial Brook et al.33)
vasoconstriction in healthy adults
Respiratory
2000 Targeting aerosol deposition in patients with cystic fibrosis Laube et al.57)
2001 Air pollution and hospital admissions for respiratory conditions in Rome, Italy Fusco et al.42)
2007 Tuberculosis among workers exposed to free silica dust Tiwari et al.48)
2008 A 10-year time-series analysis of respiratory and cardiovascular morbidity in Nicosia, Middleton et al.49)
Cyprus: the effects of short-term changes in air pollution and dust storms
2011 Quartz exposure and increased respiratory symptoms among coal mine workers in Mamuya et al.16)
Tanzania
2012 Potential determinants of coal workers' pneumoconiosis, advanced pneumoconiosis, Laney et al.15)
and progressive massive fibrosis among underground coal miners in the United States
2016 Risk of occupational exposure to asbestos, silicon, and arsenic, on pulmonary Bhattacharjee et al.45)
disorders: understanding the genetic-epigenetic interplay and future prospects
2018 Effects of particulate matter on allergic respiratory diseases Wu et al.21)
Neurology
2005 Effects of Asian dust storm events on daily stroke admissions in Taipei, Taiwan Yang et al.54)
2008 Air pollution, cognitive deficits, and brain abnormalities: A pilot study with children Calderón-Garcidueñas
and dogs et al.52)
2009 Air pollution: mechanisms of neuroinflammation and CNS disease Block51)
2013 Asian dust storm events are associated with an acute increase in stroke hospitalisation Kang et al.55)
2018 Air pollution and stroke Lee et al.53)
www.ksmp.or.kr
Progress in Medical Physics Vol. 29, No. 3, September 2018 87
Rescue the Effects of Particulate Matter treated with DHA for seven days before they were sub-
jected to ODE. The results were compared with mice that
The inhalation of PM led to inflammatory lung diseases were subjected to ODE alone, and it was found that mice
and asthma, and consequently elicits a systemic disease treated with DHA showed major reductions in neutrophil
manifestation, such as osteoporosis and fracture. System- infiltration and pro-inflammatory cytokine/chemokine
atic bone loss was a major health problem and utmost production in ODE-induced bronchial alveolar lavage. It
attention was required to deal with this malady. Bone loss was suggested that the DHA served to reduced airway in-
has been a linked feature with air inflammatory diseases, flammatory diseases. Hence, DHA supplementation may
yet there was no strategies designed to cease their progres- be an effective way to reduce air inflammatory diseases
sion. Vitamin D was essential for bones, and its deficiency caused by PM.68)
causes bone loss and hyperparathyroidism. Experiments
were designed to discover whether the supplementation of Discussion
Vitamin D could help prevent systematic bone loss. Mice
were subjected to high/low Vitamin D supplementation for PM varies in composition, size, and nature, depending
five weeks followed by their exposure to ordinary dust ex- upon the metrological condition. The effects of these PM
tracts (ODE) or lipopolysaccharides (LPS) for three weeks. have become a major issue during the past few years, espe-
The results obtained showed no differences between the cially in Asia. Although extensive research has been con-
extent of ODE and LPS induced by inflammatory cell infil- ducted on the emergence of health issues linked to PM, to-
tration, or by the histopathology of the lungs in the cases of this-date, there was still limited available data describing
high/low vitamin D treatments. Using micro-CT analysis, it the specific PM-related health issues.
has been shown that increased vitamin D supplementation It is of extreme importance to not only identify the toxic
helped recover the loss of bone mineral density, bone vol- chemical compound in the atmosphere but to quantify its
ume, and the weakening of the bone’s micro-architecture. uptake in biological models in order to predict and evalu-
With the treatment of vitamin D, bone-reabsorbing os- ate the associated potential risk. Inhalation of polyhexa-
teoclasts decreased as well. However, reduced Vitamin D methylene guanidine was quantified using radio-isotope
supplementation did not accomplish any of the results that labelled method on nuclear imaging system by Jeon et
were accomplish using increased Vitamin D supplementa- al.69). These radiolabeling technique would be useful for
tion. Thus, increased concentrations of Vitamin D proved imaging PM.
successful for the protection against systematic bone loss Imaging was significant in understanding, diagnosis, and
but did not succeed in preventing and providing protection treatment of various diseases, ailments, and inflamma-
67)
against airway inflammation caused by ODE or LPS. An- tions. Undoubtedly, imaging has been one of the most im-
other attempt expended in formulating a preventive thera- portant scientific tools of the twenty first century. Nuclear
peutic strategy to overcome the effects of PM indicated that medicine imaging technique such as PET or SPECT could
PM originated from concentrated animal feeding opera- provide the information of bio distribution of PM, and their
tions (CAFO’s). CAFO’s caused airway inflammatory dis- effects on human.
eases in exposed workers. Omega-3 fatty acids were found
to attenuate inflammatory processes. A pilot research study Acknowledgements
was conducted to identify whether it could reduce the air-
way inflammation caused by organic dust. Human body This work was supported by the Ministry of Health and
cells were pretreated with omega-3 fatty acid docosahexae- Welfare (HO15C0003, PI: Jin Su Kim), and by the Korean
noic acid (DHA), and were then subjected to dust from Institute of Radiological and Medical Sciences funded by
CAFO’s (ODE), and were reported to reduce ODE-induced the Ministry of Science and ICT (50536-2018, PI: Yong Jin
inflammatory cytokine production. Moreover, mice were Lee). However, the funders had no role in the conceptual-
www.ksmp.or.kr
88 Javeria Zaheer, et al:Imaging the Effect of Particulate Matter
ization, design, data collection and analysis, or decision to 8. Bućko MS, Magiera T, Johanson B, Petrovský E, Pesonen
publish. LJ. Identification of magnetic particulates in road dust ac-
cumulated on roadside snow using magnetic, geochemi-
Conflicts of Interest cal and micro-morphological analyses. Environ Pollut.
2011;159: 1266-1276.
The authors have nothing to disclose. 9. Takada H, Onda T, Harada M, Ogura N. Distribution and
sources of polycyclic aromatic hydrocarbons (PAHs) in
Availability of Data and Materials street dust from the Tokyo metropolitan area. Sci Total En-
viron. 1991;107: 45-69.
All relevant data are within the paper and its Supporting 10. Sofilic T, Rastovcan-Mioc A, Cerjan-Stefanovic S, Novosel-
Information files. Radovic V, Jenko M. Characterization of steel mill electric-
arc furnace dust. J Hazard Mater. 2004;109: 59-70.
Ethics Approval and Consent to Participate 11. Wheatley AD, Sadhra S. Occupational exposure to diesel
exhaust fumes. Ann Occup Hyg. 2004;148: 369-376.
The study was approved by the institutional review board 12. Snider G, Weagle C. L, MurdymootooK, et al. Variation in
(IRB approval number; 2018-0016). global chemical composition of PM 2.5: emerging results
from SPARTAN.Atmos. Chem. Phys. 2016;16: 9629-9653.
References 13. Chen W, Liu Y, Wang H, Hnizdo E, et al. Long-term expo-
sure to silica dust and risk of total and cause-specific mor-
1. Kang D, Kim JE. Fine, ultrafine, and yellow dust: emerging tality in Chinese workers: a cohort study. PLoS Med. 2012;
health problems in Korea. J Korean Med Sci. 2014;29: 621- 9(4): e1001206.
622. 14. Jeong SH, Jeong HE, Byong KS, et al. Comparison of air
2. Shepherd M. NARSTO report Ch 1.Perspective for mang- pollution and the prevalence of allergy-related diseases
ing PM. US, Mexico, Canada. NARSTO 2004.53-68. in Incheon and Jeju City. Korean J Pediatrics 2011;54: 501-
3. Jemmett-Smith BC, Marsham JH, Knippertz P, Gilkeson 506.
CA. Quantifying global dust devil occurrence from meteo- 15. Laney AS, Petsonk EL, Hale JM, Wolfe AL, Attfield MD. Po-
rological analyses. Geophys Res Lett. 2015;42: 1275-1282. tential determinants of coal worker’s pneumoconiosis, ad-
4. Wang X, Cheng H, Che H, et al. Modern dust aerosol avail- vanced pneumoconiosis, and progressive massive fibrosis
ability in northwestern China. Sci Rep. 2017;7: 8741. among underground coal miners in the United States,
5. Kandler K, Benker N, Bundke U. Chemical composition 2005-2009. Am J Public Health. 2012;102 (Suppl 2): S279-
and complex refractive index of saharan mineral dust at 283.
Izaña, Tenerife (Spain) derived by electron microscopy. 16. Mamuya SH, Moen B, Bratveit M. Quartz exposure and in-
Atmospheric Environ. 2007;41: 8058-8074. creased respiratory symptoms among coal mine workers
6. Maxwel-Meier K, Weber R, Song C, Orsini, Ma Y. Inor- in Tanzania. East Afr J Public Health. 2011;8: 190-195.
ganic composition of fine particles in mixed mineral dust- 17. Moreno T, Kojima T, Querol X, et al. Natural versus an-
pollution plumes observed from airborne measurements thropogenic inhalable aerosol chemistry of transbound-
during ACE-Asia. J Geophys Res: Atmospheres 2004;109: ary East Asian atmospheric outflows into western Japan.
D19S07. Scie Total Environ. 2012;424: 182-192.
7. Farfel MR, Orlova AO, Lees PSJ, Rohde C, Ashley PJ, Chi- 18. Neghab M, Mohraz MH, Hassanzadeh J. Symptoms of
solm JJ. A study of urban housing demolitions as sources respiratory disease and lung functional impairment as-
of lead in ambient dust: demolition practices and exterior sociated with occupational inhalation exposure to carbon
dust fall. Environmental Health Perspectives. 2003;111: black dust. J Occup Health. 2011;53: 432-438.
1228-1234. 19. Sahle W, Krantz S, Christensson B, Laszlo I. Preliminary
www.ksmp.or.kr
Progress in Medical Physics Vol. 29, No. 3, September 2018 89
data on hard metal workers exposure to tungsten oxide sponses in healthy adults during controlled air pollution
fibres. Sci Total Environ. 1996;191: 153-167. exposures. Environ Health Perspectives 2005;113: 1052-
20. Bharadwaj P, Burney J. Cognition impact of sand and dust 1055.
storms highlights future research needs?. Lancet. Planet 33. Brook RD, Brooke JR, Urch B, et al. Inhalation of fine par-
Health. 2018;2(5); e196-e197. ticulate air pollution and ozone causes acute arterial vaso-
21. Wu J.Z, Dan-Dan G, Lin-fu Z, Ling Y, Ying Z, Qi Yuan L. Ef- constriction in healthy adults. Circ. 2002;105: 1534-1536.
fects of particulate matter on allergic respiratory diseases. 34. Peters A, Stephenie VK, Margit H, et al. Exposure to traf-
Chronic Dis Transl Med. 2018;4: 95-102. fic and the onset of myocardial infarction. New England J
22. Chen B, Kan H. Air pollution and population health: a Med. 2004;351: 1721-1730.
global challenge. Environ Health Preventive Med. 2008;13: 35. Ueda K, Shimizu A, Nitta H, Inoue K. Long-range trans-
94-101. ported Asian dust and emergency ambulance dispatches.
23. Kolpakova AF, Sharipov RN, Kolpakov FA. Air pollution by Inhalation Toxicol 2012;24: 858-867.
particulate matter as the risk factor for the cardiovascular 36. Lee J-T, Kim H, Cho YS, et al. Air pollution and hospital
diseases. Gigiena i Sanitariia. 2017;96: 133-137. admissions for ischemic heart diseases among individu-
24. Tsai S-S, Goggins WB, Chiu HF, Yang C-Y. Evidence for an als 64+ years of age residing in Seoul, Korea. Arch Environ
association between air pollution and daily stroke admis- Health: Int J. 2003;58: 617-623.
sions in Kaohsiung, Taiwan. Stroke. 2003;34: 2612-2616. 37. Tam WWS, Wong TW, Wong AHS. Effect of dust storm
25. Pinault LL, Weichenthal S, Crouse DL, et al. Associations events on daily emergency admissions for cardiovascular
between fine particulate matter and mortality in the 2001 diseases. Circ. 2012;76: 655-660.
Canadian Census Health and Environment Cohort. Envi- 38. Mueller-Anneling LJ, O’Neill ME, Thorne PS. Biomonitor-
ron Res. 2017;159: 406-415. ing for assessment of organic dust-induced lung inflam-
26. Nemery B, Hoet PHM, Nemmar A. The Meuse valley fog of mation. Eur Resp J. 2006;27: 1096-1102.
1930: an air pollution disaster. Lancet 2001;357: 704-708. 39. Kang J-H, Keller JJ, Chen C-S, Lin H-C. Asian dust storm
27. Logan WPD. Mortality in the London fog incident, 1952. events are associated with an acute increase in pneumo-
Lancet 1953;261: 336-338. nia hospitalization. Ann Epidemiol. 2012;22: 257-263.
28. Brook RD, Franklin B, Cascio W, et al. Air pollution and 40. Burnett RT, Smith-Doiron M, Stieb D, Cakmak S, Brook JR.
cardiovascular disease. A statement for healthcare profes- Effects of particulate and gaseous air pollution on cardio-
sionals from the expert panel on population and preven- respiratory hospitalizations. Arch Environ Health: Int J.
tion science of the American Heart Association.Circ. 2004; 1999;54: 130-139.
109: 2655-2671. 41. Schwartz J. PM10 ozone, and hospital admissions for the
29. Milojevic A. Paul W, Ben A, et al. Short-term effects of air elderly in Minneapolis-St. Paul, Minnesota. Arch Environ
pollution on a range of cardiovascular events in England Health: Int J. 1994;49: 366-374.
and Wales: case-crossover analysis of the MINAP data- 42. Fusco D, Forestiere F, Michelozzi P, et al. Air pollution and
base, hospital admissions and mortality. Heart. 2014;100: hospital admissions for respiratory conditions in Rome,
1093-1098. Italy. Eur Resp J. 2001;17: 1143-1150.
30. Middleton N, Panayiotis Y, Savvas K, et al. A 10-year time- 43. Wagner GR. Asbestosis and silicosis. Lancet. 1997;349:
series analysis of respiratory and cardiovascular morbid- 1311-1315.
ity in Nicosia, Cyprus: the effect of short-term changes in 44. Middleton EL. Industrial pulmonary disease due to the in-
air pollution and dust storms. Environ Health 2008;7: 39. halation of dust with special reference to silieosis. Lancet.
31. Pope IC, Burnett RT, Thun MJ, et al. Lung cancer, cardio- 1936;139: 59-64.
pulmonary mortality, and long-term exposure to fine par- 45. Bhattacharjee P, Paul S, Bhattacharjee P. Risk of occupa-
ticulate air pollution. JAMA. 2002;287: 1132-1141. tional exposure to asbestos, silicon and arsenic on pul-
32. Urch B, Frances S, Paul S, et al. Acute blood pressure re- monary disorders: understanding the genetic-epigenetic
www.ksmp.or.kr
90 Javeria Zaheer, et al:Imaging the Effect of Particulate Matter
interplay and future prospects. Environ Res. 2016;147: 425- into the blood circulation in humans. Circ 2002:105:1411-
434. 414.
46. Michel O, Kipps J, Duchateau J, et al. Severity of asthma is 60. Berridge M.S., Lee Z., Heald D.L. Pulmonary distribution
related to endotoxin in house dust. Am J Resp. Crit Care and kinetics of inhaled 11C-tiamcinolone acetonide. J Nucl
Med. 1996;154: 1641-1646. Med.2000;41: 1603-1611.
47. Lin M-T, Chew TK, Chun C-C, et al. Association of meteo- 61. Visser TJ, Van WA,Doze P, et al. Characterisation of β2-
rological factors and air NO2 and O3 concentrations with adrenoceptors, using the agonist 11C-formoterol and posi-
acute exacerbation of elderly chronic obstructive pulmo- tron emission tomography. Eur J Pharmacol. 1998;361: 35-
nary disease. Sci Rep. 2018;8: 10192. 41.
48. Tiwari RR, Sharma YK, Saiyed HN. Tuberculosis among 62. Guenther KJ, Yoganathan S, Garofalo R, et al. Synthesis
workers exposed to free silica dust. Indian J Occup and and in vitro evaluation of 18F- and 19F-labeled insulin: A
Environ Med. 2007;11: 61-64. new radiotracer for PET-based molecular imaging studies.
49. Middleton NJ. Desert dust hazards: A global review. Aeo- J Med Chem. 2006;49: 1466-1474.
lian Res. 2017;24: 53-63. 63. Iozzo P, Osman S, Glaser M, et al. In vivo imaging of insu-
50. Zhang ZF, Yu SZ, Zhou GD. Indoor air pollution of coal lin receptors by PET: preclinical evaluation of 125I and 124I
fumes as a risk factor of stroke. Shanghai. Am J Public labelled human insulin. Nuc Med Biol. 2002;29: 73-82.
Health. 1988;78: 975-977. 64. Dolovich MB. 18F-FDG positron emission tomographic
51. Block ML, Calderón-Garcidueñas. Air pollution: mecha- imaging of pulmonary functions, pathology, and drug de-
nisms of neuroinflammation and CNS disease. Trends in livery. Proc Am Thorac Soc 2009;6: 477-485.
Neurosci. 2009;32: 506-516. 65. Tarkin JM, Joshi FR, Rudd JH. PET imaging of inflamma-
52. Calderón-Garcidueñas L, Mora-Tiscareño A, Ontiveros E, tion in atherosclerosis. 2014;11: 443-57.
et al. Air pollution, cognitive deficits and brain abnormali- 66. Capitanio S, Nordin AJ, Noraini AR, Rossetti C. PET/CT in
ties: A pilot study with children and dogs. Brain and Cog- nononcological lung diseases: current applications and
nit. 2008;68: 117-127. future perspectives. Eur Resp Rev. 2016;25: 247-258.
53. Lee KK, Miller MR, Shah ASV. Air pollution and stroke. J 67. Dusad A, Geoffrey MT, Lynell WK, et al. Vitamin D supple-
Stroke. 2018;20: 2-11. mentation protects against bone loss following inhalant
54. Yang C-Y, Chen Y-S, Chiu H-F, Goggins W. Effects of Asian organic dust and lipopolysaccharide exposures in mice.
dust storm events on daily stroke admissions in Taipei, Immunol Res. 2015;62: 46-59.
Taiwan. Environ Res. 2005; 99(1):79-84. 68. Nordgren TM, Friemel TD, Heires AJ, et al. The omega-3
55. Kang JH, Liu TC, Keller J, Lin HC. Asian dust storm events fatty acid docosahexaenoic acid attenuates organic dust-
are associated with an acute increase in stroke hospitali- induced airway inflammation. Nutrients. 2014;6: 5434-54.
sation. J Epidemiol Commun Health. 2013;67: 125-131. 69. Shim H.E, Lee J.Y, Lee C.H, et al. Quantification of inhaled
56. Scheuch G, Bennett W, Borgström L, et al. Deposition, im- aerosol particles composed of toxic house hold disinfec-
aging, and clearance: what remains to be done?. J Aerosol- tant using radioanalytical method. Chemophere.2018;207:
Med Pulm Drug Deliv 2010; 23 (Suppl 2):S39-57. 649-654.
57. Laube BL, Jashnani R, Dalby RN, Zeitlin PL. Targeting 70. Baldacci S, Maio S, Cerrai S, et al. Allergy and asthma: Ef-
aerosol deposition in patients with cystic fibrosis. Chest. fects of the exposure to particulate matter and biological
2000;118: 1069-1076. allergens. Resp Med. 2015;109: 1089-1104.
58. EC Pratt, TM Shaffer, J Grimm. Nanopart icles and 71. Jalbert I, Golebiowski B. Environmental aeroallergens and
radiotracers:advances towards radionanomedicine. Wiley allergic rhino-conjunctivitis. Curr Opin Allergy Clin Im-
Interdisciplinary Reviews: Nanomedicine and Nanobio- munol 2015;15: 476-481.
technology.2016;8: 872-890. 72. Tian Y, Xiao X, Yiqun W, et al. Fine particulate air pollu-
59. AD Nemmar, PHM Hoest, et al. Passage of inhaled particle tion and first hospital admissions for ischemic stroke in
www.ksmp.or.kr
Progress in Medical Physics Vol. 29, No. 3, September 2018 91
Beijing, China. Sci Rep. 2017;7(1): 3897. gen dioxide concentration and the relative risk of develop-
73. Akbarzadeh MA, Khaheshi I, Sharifi A, et al. The associa- ing STEMI: A case-crossover design. Environ Res. 2018;
tion between exposure to air pollutants including PM10, 161: 299-303.
PM2.5, ozone, carbon monoxide, sulfur dioxide, and nitro-
www.ksmp.or.kr