Plenary Workshop of the UK Natural Dust & Health Network Meeting

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Plenary Workshop of the UK Natural Dust & Health Network
Meeting Notes
Key to notes
Q
Question
A
Answer
S
Statement
Please refer to list of delegates for expertise of discussion participants
Setting the scene
Talks:
1. Claire Horwell – Mineralogy and Volcanology.
Key Points:
 Objectives of field:
i. To use mineralogy and geochemistry to make rapid assessments of the
potential health hazard of natural mineral particles (NMPs)
ii. To understand why a mineral or dust may trigger a pathogenic
respiratory response.
 Questions that mineralogy can answer:
i. Is the dust small enough to enter the lung?
ii. What is the composition of the dust?
iii. Is shape relevant (e.g. fibrous)?
iv. Is the surface of the dust reactive?
v. Are individual particles ‘pure’?
vi. Is the crystalline structure relevant?
 Answers:
i. Grain size: for volcanoes, quantity of respirable (<4 um) fraction varies
from 0-17%.
ii. Composition: Techniques such as SEM-EDS allow characterisation of
composition of individual particles.
iii. Shape: Also done by techniques such as SEM but can automate process
with image analysis.
iv. Reactivity: Volcanic silica appears not to generate silica surface
radicals but does generate hydroxyl radicals through the Fenton
Reaction – ash is rich in reduced iron – unusual for crustal dusts. Ash
types containing more iron generate more radicals.
v. Purity: Crystalline silica in ash may be modified by more inert minerals
by:
1. surface occlusion by glass
2. intergrowth of silica with other minerals
3. substitution of Si from atomic structure by Al & Na.
We have confirmed 2 & 3. Work commencing on 1. in 2008.
vi. Structure: we have found both alpha and beta cristobalite –
may
have toxicological relevance.
2. Ken Donaldson – The Toxicology of NMP
Key Points:
 What diseases do particles cause or worsen? Table of different parts of lung with
lung site, disease, setting (Occ/Env) and exemplar particles such as coalmine
dusts.
 Exposure effects based on the occupational paradigm:
o People exposed to high doses (mg/m3) in peaks followed by zero exposure
in the workplace.
o Particles: silica, asbestos, welding fume, nuisance dusts
o Healthy worker effect – ill people leave. Predominantly healthy males < 65
years old.
o Responses: Pneumoconiosis, COPD, cancer, asthma.
 Exposure effects based on environmental paradigm (PM10)
o Exposure very low (tens of ug/m3) – constant with peaks.
o Exposure to urban PM10, containing combustion–derived particles.
o Everyone exposed but only susceptible, e.g. aged and ill, affected.
o Responses: COPD and asthma and exacerbation of cardiovascular disease
and cancer.
 NMPs don’t necessarily fit in with either of the environmental or occupational
paradigms.
 Factors contributing to toxic response: concentration and length of exposure
contribute to dose. Intrinsic toxicity important too.
 General scheme of what happens in the lung with harmful particles: if clearance of
particles doesn’t occur, may result in inflammation, oxidative damage, tissue
injury and then disease.
 Biologically effective dose (BED) important. We are poor at measuring BED
metrics – different metrics used for different particles. Table showing particle,
BED and current metric. Move to have BED as metric rather than mass.
 Inflammation plays a central role for occupational particles, leading to different
disease outcomes depending on the part of the lung which is affected.
 Inflammation also important for environmental particles too.
 Oxidative stress – particles intrinsically have the ability to cause oxidative stress
which then causes inflammation.
 Testing approaches: depends on aim (screening, mechanisms, regulatory)
o Characterising the physico/chemistry - structure:activity paradigm
(mineralogy integration – see Horwell’s presentation).
o In vitro (cell-free) e.g. surface reactivity (see Horwell’s presentation)
o In vitro (cells) – endpoints must be pathophysiologically relevant.
o In vivo assessment.
 Example of inhalation study with NMP: IOM/Edinburgh Soufrière Hills in vivo
study. Importance of using controls to contextualise response e.g. TiO2. Need to
compare it with coal mine dust and quartz.
 Summing up.
o Some natural dusts are also occupational dusts e.g. coalmine, asbestos. Do
we need to treat them separately?
o Do environmental exposures cause disease?
o How may people at risk? If not substantial then unlikely to get funding.
Need to know documented burden of ill health.
Q: Ben Williamson:
Should we study dust which is extremely fresh as this is what people are exposed to?
A: Ken Donaldson:
Quartz ages rapidly over a few hours so most people exposed to aged particles.
A: Bice Fubini:
Mechanisms of formation of fresh particulates might be similar with different NMPs and
combustion particles. Also volcanic particles are similarly formed to rock blasting
Q: Mike Moore:
Coastal areas have sea water droplets – viral soup – probably in aerosol at nano size. Will
they interact with NMPs and coat them which might change reaction?
A: Ross Anderson:
No epidemiological information to show that seaside areas have higher incidence of
disease.
A: Ken Donaldson:
Concentrated Edinburgh air (high salt) showed no effects.
A: Jon Ayres:
Coastal asthma known
A: Ross Anderson:
Hard to study as would need so many data to untangle individual effects of constituents –
would run out of statistical power.
3. Peter Baxter – Health effects of coarse airborne particles (2.5-10um)
Key Points:
 Crustal particles – volcanic ash, soil-derived in urban air, dust storms and wind-blown
ash
 (Review Refs: Horwell & Baxter, Bull. Volcanol. 2006; Brunekreef &
Forsberg, Eur Respir J, 2005).
 Review of Mt St Helens eruption, USA, May 1980: loggers had greatest exposure.
Confusion over silica content. Acute respiratory effects observed.
 Review of Soufrière Hills eruption, Montserrat, 1995-present. Unprecedented
exposure to volcanic particulate matter. Summary of studies done:
 Asthma studies in school children, 1998 & 2008
 Cristobalite hazard quantified in 1999 & 2003 papers
 Cumulative exposure assessment 1996-2000
 Toxicological studies by different UK labs.
 Silicosis risk quantified.
 Chest Xray and lung function studies done in adults and children.
 Factors affecting lung toxicity of silica particles (covered by Horwell & Donaldson’s
presentations)
 Health hazards of volcanic ash review summary (Horwell & Baxter 2006)
 Few epidemiological or clinical studies around the world
 Mostly poor characterisation of ash samples
 Inadequate exposure information
 Only MSH & SHV have had detailed studies
 Variable results but asthma outbreak seen at Cerro Negro, Nicaragua, 1992.
 Effects of coarse PM on short-term mortality. Cardiovascular disease seen in US (nonvolcanic studies).
 Effects of coarse PM on long-term mortality. Six studies found effect for fine fraction.
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Effects of coarse PM on short-term morbidity. In several studies, coarse fraction is a
better predictor than fine fraction for daily numbers of respiratory admissions.
Effects of dust storms and wind blown dust: no consistent findings.
Summary – is volcanic ash a model for crustal particle toxicity? But many different
forms of NMPs. COMEAP report was based on PM2.5 and may be influenced by cofactors such as sulphate.
4. Anthony Seaton – NMPs: risks and their controls
Key Points:
 General rules for reduction of risk from inhaled substances:
 Good information for exposed public,
 Total avoidance of exposure (substitution of materials or evacuation),
 Exposure reduction – limiting duration, reduce activities, personal protection.
 Then audit for effectiveness of measures.
 What are the health effects of oil shale exploration? Seaton did study. Am J Indust
Med, 1986, 9, 409.
 In order to prevent disease you don’t need to know the cause of disease.
 Coal diseases affected by several factors such as smoking and the coal rank.
 Air quality standards and guidelines: Problems with:
 Different dust compositions, some of which are mixed dust.
 Difficulty of regulation, monitoring and compliance
 Lack of epidemiology.
 Would be possible to publish a management strategy based on analogous
mineralogical, epidemiological and toxicological evidence – done on Montserrat.
Main Group Discussion
Output – a document highlighting main areas for future research in the area.
Q: Peter Baxter
Can we use volcanological particles as a model transferable to other NMPs and maybe urban
air pollution?
A: Bill Rose
Volcanological particles are affected by distance from volcano and size. He is looking at ‘total
size distribution’ – linked to mechanism of formation e.g. milling in pyroclastic flows. Mature
particles (that don’t fall out from an ash cloud immediately) fall into different classes:
 Particles with fresh, new surfaces > 5um.
 Sulphates < 0.5 um diameter, liquid droplets formed during eruption.
 ~ 1um class – elemental particles (some soluble, e.g. halides, sulphates, metals
(akin to fumarole environment)). Diverse with each volcano having a different
signature e.g. vanadium, thallium, rhenium, copper, molibdinum, lead, tungsten.
Can be modelled thermodynamically. Source is subducted oceanic slab and
subsequent interaction of wet slab with mantle as slab melts. Metals and acids may
coat larger particles.
Hydroxyl radicals seen in plume from Hekla volcano (Iceland) – may be formed in eruption
and then frozen or form in stratosphere with iron interaction and H2O2 found in atmosphere.
Plume transforms with time. (Rose et al, 20061)
Q: Ben Williamson
Could charging affect radical formation and aggregation from electrical storms in plume?
S: John Ayres
Charging also affects deposition in the lung.
A: question not answered but general agreement that mechanism potentially possible.
S: Steve Smith
In relation to Bill Rose’s statement re. different fractions:
There are parallels with urban size distributions and reactions e.g. aqueous environments.
Fractions known as: Nucleation mode, accumulation mode and coarse (>2.5 um) mode.
S: Bill Rose
By the time one samples in an aircraft, often several hours after eruption so distribution
skewed to fine mode. Also, silicate mode is dominant early on in the clouds, then other modes
stand out later on.
Q: Bice Fubini
Temperature formation may be important - ash generated is hot – is there a parallel to
incinerators?
A: Bill Rose
There may be a parallel with forest fires - also creates stratospheric cloud with ice nuclei.
S: Bice Fubini
Surface of the particle would be different because silica crushed is very fresh.
Q: Bill Rose
Could we do lab work which shows newly created ash surfaces and simulate reactions
between particles e.g. explosive vesiculation (experiments could be done on dome rock at
Prof. Don Dingwell’s labs in Munich). Might produce different results from grinding (e.g.
work published in Horwell et al. 20032).
Q: Anthony Seaton
How are stratospheric interactions (e.g. those observed in Rose et al. (20061) appropriate to
human health exposure?
A: Bill Rose
We may not have many other choices but to look at stratospheric interactions. It is hard to
collect particles, especially as volcanologists usually collect samples close to volcanoes, and
distally may be low concentration. The idea of using aircraft is also hard as can damage
engines so hard to set up experiments. Observations of Hekla plume happened by mistake.
Heavy exposure does occur distally at ground level, e.g. E. Washington following Mt St
Helens eruption, 1980.
Q: Peter Baxter
Montserrat and Mt St Helens ash not as toxic expected. Were the right samples used?
S: Claire Horwell
Variety of samples, standards and techniques used. Montserrat results much more constrained.
Toxicology results for Mt St Helens varied from very toxic to non-toxic so results not clear.
S: Jon Ayres
Aged dust vs fresh dust - hard to compare in toxicology studies as using stored dusts, which
have aged, are not reproducible.
S: John Cherrie
Difficulty with samples – airborne collected vs. bulk samples.
S: Pierre Delmelle
There are high temperature experiments of ash generation and surface reactivity. Even
exposing ash to water affects results. Surface area is fairly low compared with other crustal
dusts containing clay minerals. Also, processes in a volcanic plume are extremely different to
wind blown crustal dust, particularly due to temperatures of eruption.
S: Augusto Neri
We should distinguish between the source of the ash (plume) from the ash cloud. Plume is
complex – multi-phase mixture – v. hard to model. Ash cloud is less complex – gravity and
interaction of particles.
Q: Anna Hansell
As an epidemiologist, how can we simplify all the characteristics of particles for use by
medics? Can we use remote sensing to sample instead of trying to collect particles?
A: Rod Jones
May need a new level of instrumentation to address the impurity levels in ash.
S: Bill Rose
We already use quartz crystal micro cascade impactors – used in a plume or cloud if you can
get instrument into the cloud. Measures particles by size, measures them in situ.
S: Anthony Seaton
Epidemiologists use simple instruments (elutriator which mimics collection ability of human
lung and measures mass). Reminding us that we need to relate this to health. What is needed
is an instrument that samples biological relevant fraction with free radical generation, for
example. Sample its effect rather than what it’s made of.
S: Bice Fubini
You do need to know what it’s made of otherwise you can’t compare different samples. Need
controls too. This could build up to producing a predictive model for the toxicity of ash.
Q: Peter Baxter
How does this relate to desert dust?
A: Ed Derbyshire
Glacial system grinds rock. Other processes, frost shatter and salt crystal growth (paleolakes)
– extend over a wide range of environments. Finer than sand, the population is carried in
suspension. Silt and clay grade particles are angular (except biogenic silica, diatoms). Glacier
outwash dries out and particles are then lofted in winds and travel 1000s km. Exposure to
desert dust is a frequent chronic event, affecting high density rural populations. Deposits
show low density packing on settlement (high void ratio) especially after landslide. Dust
storms can be triggered by ploughing (machine). We also compact surfaces and reduce
vulnerability of resuspension by wind action. Clay grade quartz frequently found.
Q: Ben Williamson
What epidemiological data are there for desert regions? Have people built up genetic
resistance which wouldn’t exist with climate change (dryland advance posing new threat)?
A: Ed Derbyshire
Limited literature. Most in N. China.
A: Jon Ayres
There are several studies done on villagers in Ladakh (Northern India) where there are no
sources of industrial pollution but frequent desert dust storms. Need for systematic review of
the literature.
A: Claire Horwell
In Ladakh, there is pneumoconiosis which must be due to the dust storms.
S: Ed Derbyshire
Acute effects are important too: dust storms from Sahara for 9-10 days – needs formal
quantification of acute effects. Derbyshire is getting together a team for a pilot study on
Canary Islands. Evidence that hospital admissions for respiratory disorders coincide with dust
storms. Mineralogy varies enormously with different sources too.
Q: Pierre Delmelle
Spain Saharan impact – has anyone compared urban vs. desert dust impact?
A: Ed Derbyshire
There are single studies along Mediterranean. (CHECK) We are still observing now but there
are no good datasets. In W Med, 83 % by wet sedimentation and lower elsewhere.
S/Q: Peter Baxter
Move discussion on to coarse fraction in urban air pollution – what is it composed of?
A: Ross Anderson
Methodological issue. Time series studies based on exposure assessment over 24 hrs by urban
monitor – taken as exposure for a city on a certain day. PM2.5 is homogeneously distributed
in a city but there is greater variation in spatial distribution of coarse fraction. In Birmingham,
on windy days, PM2.5 levels decrease but coarse fraction goes up. Very different behaviour
of two components presents epidemiological challenge as never focused just on coarse
fraction. A meta-analysis of relationship between coarse fraction and mortality does show
significant associations. Problems because of low signal to noise ratio. Also, very dependent
on decent exposure estimates as we currently have little idea of what the population exposure
actually is.
Q: Ross Anderson
Is there a role for analysing autopsy lungs rather than trying to collect particles from
atmosphere to see what people have been exposed to?
A: Peter Baxter
Autopsies can also be done on grazing animals.
A: Anthony Seaton
Hard to do autopsy studies as not many post mortems done on normal people.
A: Ben Williamson
Autopsies only tells us part of the story as particles may be cleared after inducing acute
disease.
S: Ross Anderson
A large amount of coarse fraction is now brake or tyre wear so not crustal. Complicates the
issue.
S: Johan Ovrevik
Most reports show that coarse fraction more potent (cell cultures) which goes against
epidemiology.
S: Johan Ovrevik
Endotoxin may also have an effect – seen on road dusts. Well documented heterogeneity in
personal response which may be linked to susceptibility.
S: Ken Donaldson
We don’t know whether endotoxin on particles in air or grew during storage of particles in
lab.
S: Johan Ovrevik
Very few studies measuring endotoxin in outdoor air.
S: Jon Ayres
Animal dung stuffed with endotoxin and also found in cigarette smoke. May well have
differential toxicity as many different forms of endotoxin.
S: Anthony Seaton
Farmer’s lung from bacteria in fields. Also, greatest exposure is indoor at home.
S: Ken Donaldson
Effects of pollen and spores are substantial. (paper mentioned – CHECK)
S: Ross Anderson
Mould spores more important as smaller.
S: Peter Baxter
Wind storms also full of biological material
S: Ed Derbyshire
Desert dusts transport: virus, funghi and bacteria – travelling intercontinentally – Dale Griffin
review (CHECK).
Q: Rod Jones
Why is animal response different from human response?
A: Jon Ayres
Animals breath through nose whereas we breath through mouth.
A: Mike Moore
Paper in Science showing that many bacteria spend part of their life cycle in atmosphere
(CHECK paper) - so bacteria will be mixed up with dusts
S: Ross Anderson
There was a workshop last year in Bonn convened by WHO which addressed differential
toxicity of particles by source, size and chemistry. Concluded that for all particles in PM10
fraction there is evidence for health effects regardless of size, composition and source but not
enough evidence to quantify differential toxicity.(CHECK report – on web). Has
recommendations.
S: John Cherrie
Sources – environmental exposure to quarries or open cast mining.
S/Q: Peter Baxter
Move on to discussing how well we can screen particles for toxicity for biological activity,
asthma response linked to surface properties, oxidative potential or cell tests. How close are
we to being able to take a sample, and get useful information leading to further studies?
S: Jon Ayres
EPSRC nanogroup – proceedings address this topic for ultrafines in Inhalation Toxicology.
CHECK
A: Frank Kelly
Coarse particles from urban environments contain same or more oxidative potential than fine
particles on a mass basis. Shown in Dutch studies and London studies (CHECK). There is
little difference between oxidative capacity of coarse and fine particles with lung lining cells.
Thereafter, with interaction with lung cells – lots of inflammation. So toxicologists sitting on
the fence as to whether coarse or fine fractions most important. Believes it is transition metals
that are causing particles to oxidise. Biological endpoints are starting to fit with health
responses that are seen. Urban research could be very informative for NMPs
A: Jon Ayres
There is not one screening test
A: Frank Kelly
Need to compare methods directly and then choose cheapest if they show the same thing.
A: John Cherrie
We need a good formal systematic review of published literature in order to move the field
forward. We should recommend that approach. Then can identify messages. Underwhelmed
by health impact from what he’s heard. Biological/toxicology evidence is good but
epidemiology evidence is thin.
S/Q: Peter Baxter
Moving discussion on, are there developments with exposure assessment?
A: Ross Anderson
Has to go hand in hand with exposure investigations. From a health impact point of view, he
thinks necessary – World Bank done modelling exercise to model global exposure to PM10
and PM2.5 (CHECK). May be possible to do that for coarse fraction. Once you have a handle
on trends in population exposure then you can integrate better with toxicology results which
become more meaningful.
NERC Strategy
Talk by Mike Moore for Roy Harrison
Presentations of Breakout Groups giving research priorities following group discussions
Presentation Group 1
 We should be looking at “Health Impact of Environmental Exposure to Crustal
Particles” (instead of ‘NMP’)
 We recommend systematically assessing the hazard of representative crustal
minerals by mineralogical and toxicological assessment of structure/activity
relationships
 Exposure – we need to know more about airborne levels, satellite imaging and
modelling
 Response – we need to know more about health impacts
 Output – systematic review as first output – driver for direction of strategy for
research. First need to define our protocol – what dusts are included?
 Other group 1 ideas (not in presentation)
o Ross Anderson is involved in a group carrying out a review of air
pollution studies in Asia – translations being carried out. We may be able
to use some of this information.
o Claire Horwell’s definition of NMP is where the source of the particle is
natural (so includes coal, quarry dust etc).
Presentation Group 2
 What is the health burden from natural mineral dusts? On basis of what we know
– systematic review
 What is/are the best metrics of exposure?
 Mass, number, SA
 Other physical characteristics
 How best to measure these with ref to epidemiological study
 What are the mechanisms?
 Inflammation
 Oxidative stress
 Genotoxicity
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 Protein interactions
Who is susceptible?
Standard suite of particles needed
Presentation Group 3
 We need to find natural situations where we can explore the 1 um fraction –
samples can be collected from Masaya – test samples for oxidative potential.
 Independent assessment of toxicology literature needed and what papers tell us
about crustal particles. Compare with dusts that we know have strong toxic
properties.
 Capacity to respond to environmental episodes. If eruption in Iceland we are only
just 1 day downwind.
 Surface reactivity and properties, relating to toxicological endpoints. Very
important unifying theme across whole field of crustal particles.
 Existing documentation on episodes.
 Children – NMPs might have very important role and biomass burning too –
particles from biomass burning could be tested for oxidative potential.
Presentation Group 4
 Go get data – lack of information
 Sampling – what is relevant?
 Toxicity – what makes a particle toxic?
 Importance to human health? How big is the problem? Review available
literature.
Presentation Group 5
 4 types of NMP that we should consider: (volcanic, crustal, biogenic and fire)
 With volcanic – epidemiology, toxicology and characterisation done for MSH &
Montserrat
 Epidemiology may be a priority
 Characterisation – standard materials and effects of ageing
 Crustal – need for epidemiological studies and characterisation studies and what
about genetics and resistivity?
 Fire – minerals generated by burning.
Group discussion
 Do we include biomass burning within this group? Group decides it is a big separate
issue. Related to combustion.
 Do we include biogenic dust? Yes.
 What makes particles toxic? … we need a better understanding of why quartz is toxic.
 Idea of comparing mixed dusts with standard mixed dusts rather than using
single mineral controls. Problem is – maybe mixed dusts just aren’t very toxic
because of other minerals.
 Silica (quartz) is unusual because causes its own disease. ASK BICE FOR
CLARIFICATION
 What about other minerals? Are silicates a vector for transporting iron into the lung?
 What about transition metals and redox active metals? Iron, zinc, copper, arsenic.
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Exposure – what should we try to measure? Probably PM10 as we are interested in the
coarse (2.5-10 um) fractions.
Surface area – perhaps have a standardised methodology but not sure what is best way.
Differences between BET and other techniques – we need to know why numbers don’t
agree. Mass and number are easiest to measure in the field.
Epidemiology – what studies should we do to look at burden of ill health related to crustal
particles?
 Need better exposure measurements
 Saharan dust would be a good study as know that it happens frequently and if
have conviction that acute health effects might occur. School children good to
study as can get school set up for study. Canaries well positioned (Las Palmas
7th biggest city in Spain). EU Funding? John Cherrie said new dust monitors
which are low cost (in development CHECK). May get money under climate
change – desertification.
 Possibilities in NW China – harder environment but attractive because millions
of people and potential population affected is much higher than Saharan
exposure.
Systematic review – divvy up between the group - decide at 3rd meeting
A panel of particles which are well characterised mineralogically and toxicologically.
What would it comprise?
 Samples would need to be respirable – crushed then aerosolised and collected
in a high volume aerosol sampler.
 Come up with an average crust composition for comparison.
 Iron oxides, iron rich minerals, volcanic glass (dominant phase), plagioclase,
hornblende, quartz, cristobalite, clays. French group which has mapped this
(Durant CHECK). Upper Pleistocene loess of China is very similar in
composition to the average crustal composition (Ed CHECK).
 Do nanoparticles exist in crustal emissions?
The Future
 Listserv
 In toxicology, nano is the way forward. Lots of funding available.
o Naonrisk (South Ken) natural particles may be included in that study
(CHECK)
o Rob Martin study used TEM on plume silicates
References
W. I. Rose, G. A. Millard, T. A. Mather, D. E. Hunton, B. Anderson, C. Oppenheimer, B. F. Thornton,
T. M. Gerlach, A. A. Viggiano, Y. Kondo, T. M. Miller and J. O. Ballenthin, J. Geophys. Res.,
2006, 111, D20206.
C. J. Horwell, I. Fenoglio, K. V. Ragnarsdottir, R. S. J. Sparks and B. Fubini, Environmental
Research, 2003, 93, 202-215.
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