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5. HEALTH IMPACTS OF ULTRAFINE PARTICLES

5.1 GENERAL OVERVIEW ON HEALTH IMPACTS OF TSP, PM10 AND PM2.5

Over the past decade, overwhelming evidence has accumulated indicating that airborne

particles characterised as Total Suspended Particles (TSP), PM10 and PM2.5 exert a

range of adverse health effects. The identified health effects are diverse in scope,

severity, duration, and clinical significance. This diversity reflects the multiple

pathways of injury caused by air pollution and the nature of the research evidence,

which comes from epidemiological studies, human clinical exposures, animal

toxicological studies and in vitro experiments.

The evidence on the health effects of air pollution has been summarised in a number of

the state-of-the-art reviews (ATS, 1996a; ATS, 1996b; Holgate and Maynard, 1999) as

well as in two recent U.S. EPA criteria documents (USEPA, 1996; USEPA, 1999). This

section outlines key information on known and potential health effects associated with

airborne PM, alone and in combination with other pollutants that are routinely present

in the ambient air. The information highlighted here summarizes:

� Nature of the effects that have been reported to be associated with ambient PM;
� Sensitive subpopulations that appear to be at greater risk to such effects; and
� Integral evaluation of the health effects evidence.

Nature of the effects

The key health effects categories associated with PM include:

� Premature mortality;
� Aggravation of respiratory and cardiovascular disease (as indicated by increased

hospital admissions and emergency room visits, school absences, work loss days,

and restricted activity days);

� Changes in autonomic nervous system function and cardiovascular risk factors such
as blood pressure, C-reactive protein or endothelial dysfunction

� Changes in systemic blood markers
� Changes in lung function and increased respiratory symptoms;
� Changes to lung tissues and structure; and
� Altered respiratory defence mechanisms.

Most of these effects have been consistently associated with ambient PM

concentrations, which have been used as a measure of population exposure in a number

of community epidemiological studies. Additional information and insight into these

effects is provided by animal studies, in vitro toxicology, and controlled-human
exposures to various constituents of PM conducted at higher-than-ambient

concentrations. Although mechanisms by which particles cause effects have not been

elucidated, there is general agreement that the cardio-respiratory system is the major

target of PM effects.

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Sensitive subpopulations

The epidemiological studies provide evidence that several subpopulations are more

susceptible to the effects of air pollution containing PM. The observed effects in these

subpopulations range from the decreases in pulmonary function reported in children to

increased mortality reported in the elderly and in individuals with cardiopulmonary

disease. Such subpopulations may experience effects at lower levels of PM than the

general population, and the severity of effects may be greater.

The subpopulations that appear to be at greatest risk due to exposure to ambient PM

include:

� Individuals with respiratory disease (e.g., COPD, acute bronchitis) and
cardiovascular disease (e.g., ischemic heart disease) are at greater risk of premature

mortality and hospitalisation.

� Individuals with infectious respiratory disease (e.g., pneumonia) are at greater risk
of premature mortality and morbidity (e.g., hospitalisation, aggravation of

respiratory symptoms). Also, exposure to PM may increase individual susceptibility

to respiratory infections.

� Elderly individuals are also at greater risk of premature mortality and
hospitalisation for cardiopulmonary causes.

� Children are at greater risk of increased respiratory symptoms and decreased lung
function.

� Asthmatic children and adults are at risk of exacerbation of symptoms and increased
need for medical attention.

Integral evaluation of health effects evidence

Community epidemiological studies provide evidence that serious health effects are

associated with exposures to ambient levels of PM characterised as TSP, PM10 and

PM2.5 and found in contemporary urban airsheds at concentrations below current PM

standards (USEPA, 1996). Although a variety of responses to constituents of ambient

PM have been hypothesised to contribute to the reported health effects, the relevant

toxicological and controlled human studies published to date have not identified an

accepted mechanism that would explain how such relatively low concentrations of

ambient PM might cause the health effects reported in the epidemiological literature.

However, the toxicological studies tend to show that particles become more toxic per

unit mass as their size decreases. Thus, attention is focused upon surface area or particle

number per unit mass, rather than mass fraction.

Studies on particle mass concentration (PM10 and PM2.5) indicate that for particle mass

there is no threshold in particle concentrations below which health would not be

jeopardised. This is presented in the World Health Organization Guidelines for Air

Quality (WHO 1999), which shows a linear relationship between PM10 and PM2.5 and

various health indictors (including mortality, hospital admissions, bronchodilator use,

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Table 5.3.2.3 Summary on animal in-vivo studies

Ref Groups

studied

Effects studied Study Description Findings/ Conclusions

Baggs et al.,

(1997).

Rats Pulmonary

inflammatory

Male Fisher 344 rats were exposed for 6 hours

a day, 5 days a week, for 3 months to 1)

filtered air (control); 2) TiO2-D, 20 nm

particle size, 23.5 mg/m; 3) TiO2-F, 250 nm,

22.3 mg/m
3
; or 4) crystalline SiO2, a positive

control particle (similar to 800 nm particle

size, 1.3 mg/m
3
). Groups of 3-4 animals were

sacrificed at 6 and 12 months following the

completion of exposure. Pulmonary effects of

exposure were evaluated using standard

hematoxylin and eosin-stain sections,

histochemical stains for collagen, and

immunohistochemical assays for cell

turnover.

Six months after animals were exposed to SiO2, they had moderate

focal interstitial fibrosis and moderately severe focal alveolitis.

Animals exposed to TiO2-D had slightly less fibrosis. The least fibrosis

was seen in the TiO2-F group. At 1 year after exposure, fibrosis was

still present but decreased in the SiO2 group. The amount of interstitial

fibrosis in the TiO2-D- and TiO2-F-treated animals had largely returned

to untreated. Although initially irritant, TiO2-induced lesions regressed

during a 1-year period following cessation of exposure. Inhaled

ultrafine particles of TiO2 (TiO2-D, 20 nm particle size) lead to a

greater pulmonary inflammatory response than larger pigment-grade

particles (TiO2-F, 250 nm).

Brown et al.,

(2001).

Rats Respiratory Investigated proinflammatory responses to

various sizes of polystyrene particles as a

simple model of particles of varying size

including ultrafine.

There was a significantly greater neutrophil influx into the rat lung

after instillation of 64 nm polystyrene particles compared with 202-

and 535 nm particles and this was mirrored in other parameters of lung

inflammation, such as increased protein and lactate dehydrogenase in

bronchoalveolar lavage. Conclusions: the results suggest that ultrafine

particles composed of low-toxicity material such as polystyrene have

proinflammatory activity as a consequence of their large surface area.

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Ref Groups

studied

Effects studied Study Description Findings/ Conclusions

Cassee et al.,

(2002a)

Rats:

healthy &

with

pulmonary

hypertensi

on

Pulmonary

toxicity

Tested the hypothesis that secondary model

aerosols exert acute pulmonary adverse

effects in rats, and that rats with pulmonary

hypertension (PH), induced by monocrotaline

(MCT), are more sensitive to these

components than normal healthy animals. In

addition, tested the hypothesis that fine

particles exert more effects than ultrafines.

Healthy and PH rats were exposed to ultrafine

(0.07-0.10 µm; 4 x 105 particles/cm3) and fine
(0.57-0.64 µm; 9 x 103 particles/cm3)
ammonium aerosols during 4 h/day for 3

consecutive days. The mean mass

concentrations ranged from 70 to 420 µg/m3),
respectively, for ultrafine ammonium

bisulfate, nitrate, and ferrosulfate and from

275 to 410 µg/m3 for fine-mode aerosols.
Bronchoalveolar lavage fluid (BALF) analysis

and histopathological examination were

performed on animals sacrificed 1 day after

the last exposure.

Histopathology of the lungs did not reveal test atmosphere-related

abnormalities in either healthy or PH rats exposed to the ammonium

salts, or to a combination of CB + nitrate. Alveolar macrophages in

rats exposed to CB only revealed the presence of black material in

their cytoplasm. There were no signs of cytotoxicity due to the aerosol

exposures (as measured with lactate dehydrogenase [LDH], protein,

and albumin contents in BALF). Macrophages were not activated after

MCT treatment or the test atmospheres, since no changes were

observed in N-acetyl glucosaminidase (NAG). Cell differentiation

profiles were inconsistent, partly caused by an already present

infection with Haemophilus sp. The results show that at exposure

levels of ammonium salts at least one order of magnitude higher than

ambient levels, marked adverse health effects were absent in both

healthy and PH rats.

Dick et al.,

(2003).

Rats, in-
vitro

Toxicity,

Inflammation

By using four types of ultrafine particles,

carbon black (UFCB), cobalt (UFCo), nickel

(UFNi), and titanium dioxide (UFTi),

determined the attributes of the ultrafine

particles (surface area, chemical composition,

particle number, or surface reactivity) that

contribute most to its toxicity and

proinflammatory effects both in-vivo and in-
vitro.

The results suggest that ultrafine particles may cause adverse effects

via oxidative stress, and this could have implications for susceptible

individuals. Susceptible individuals, such as those with COPD or

asthma, already exhibit pre-existing oxidative stress and hence are in a

primed state for further oxidative stress induced by PM.

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