EPA PM-10 standard
Health and Environmental Effects: In 1987, EPA replaced the earlier Total Suspended Particulate (TSP) air quality standard with a PM-10 standard. The new standard focuses on smaller particles that are likely responsible for adverse health effects because of their ability to reach the lower regions of the respiratory tract. The PM-10 standard includes particles with a diameter of 10 micrometers or less (0.0004 inches or one-seventh the width of a human hair). EPA's health-based national air quality standard for PM-10 is 50 µg/m3 (measured as an annual mean) and 150 µg/m3 (measured as a daily concentration). Major concerns for human health from exposure to PM-10 include: effects on breathing and respiratory systems, damage to lung tissue, cancer, and premature death. The elderly, children, and people with chronic lung disease, influenza, or asthma, are especially sensitive to the effects of particulate matter. Acidic PM-10 can also damage human-made materials and is a major cause of reduced visibility in many parts of the U.S. New scientific studies suggest that fine particles (smaller than 2.5 micrometers in diameter) may cause serious adverse health effects. As a result, EPA is considering setting a new standard for PM-2.5.
PM10 is among the most harmful of all air pollutants. When inhaled, these particles evade the respiratory system's natural defenses and lodge deep in the lungs.
Health problems begin as the body reacts to these foreign particles. PM10 can increase the number and severity of asthma attacks, cause or aggravate bronchitis and other lung diseases, and reduce the body's ability to fight infections.
Although particulate matter can cause health problems for everyone, certain people are especially vulnerable to PM10 adverse health effects. These "sensitive populations" include children, the elderly, exercising adults, and those suffering from asthma or bronchitis.
Of greatest concern are recent studies that link PM10 exposure to the premature death of people who already have heart and lung disease, especially the elderly.
For the last several decades, high levels of outdoor air pollution have been associated with short-term increases in asthma morbidity and mortality (AAPCEH 1993; Ostro et al. 2001; Tolbert et al. 2000). Ambient hazardous air pollutants, as well as industrial releases of aldehydes, metals, isocyanates, and others have been shown to cause and trigger asthma (Leikauf et al. 1995).
Air pollution has been implicated as
one of the factors responsible for the dramatic increase in asthma incidence in
recent years. (Salvi 2001) Clinicians should be aware of the common (criteria)
air pollutants that may affect asthmatic patients. The National Ambient Air
Quality Standards (NAAQS) are set for six criteria pollutants:
Assessing the Link between PM10
Pollution and Childhood Asthma in Maricopa County, Dec 2008, www.azdeq.gov/ceh/download/Exchange%20Grant%20Summary.pdf
www.azdeq.gov/ceh/download/Health%20Project%20Report.pdf
Based
on an initial assessment of needs, available data, and analytical
capabilities
for conducting air quality modeling and establishing environmental health linkages,
ADEQ engaged researchers at Arizona State University’s (ASU)
Ira
A. Fulton School of Engineering and ASU’s Center for Health Information and
Research
(CHIR) to design and conduct a study using emissions of particulate
matter
and meteorological data provided by ADEQ to create an air quality
surface
of PM10 levels over the metropolitan Phoenix area that could be
compared
with asthma incidence data over the same geographic area and time
frame
to determine the connection between elevated levels of PM10 pollution
and
increased incidences of asthma in children.
The
study analyzed over 5,000 asthma events between January 1, 2005, and
September
30, 2006, occurring among children in a selected study area. The
study
area covered 168 census tracts in a geographic area in metropolitan
Phoenix
generally bounded by Dunlap Road to the north, 52nd Street to the east,
Elliot
Road to the south and 75th
Avenue
to the west. Each census tract included
in
the study area was located within a five-mile distance from one of the
permanent
PM10 monitors in the Phoenix area.
When
correlated with PM10 concentrations, the study showed a 13.7% increase
in the probability of
an asthma event occurring among children aged 5-18 years with changes in the
daily average PM10 from the 25th to the 75th percentile. That percentile change is equivalent to a
net increase of 26 μg/m3 of
PM10. In other words, the study revealed that the incidence of asthma events
among children 5-18 years old increased by nearly 14% when levels of PM10
pollution increased to the 75th percentile
in the study area.
Environmental studies headed by Dr. Ralph J. Delfino in the Department of Epidemiology have been conducted in San Diego and Los Angeles Counties. They have focused on the relationship of daily asthma severity to air pollutants and to aeroallergens using repeated measurements. This has involved following panels of around 20-30 asthmatics intensively for 2-3 months using peak flow meters or spirometers, and daily diaries for reporting asthma symptoms, medication use, spatial location and physical activity. The research also involves exposure assessments involving air-monitoring systems inside and outside of subject homes, and personal air samplers that subjects carry with them during their daily activities (1-4). Our first panel study showed personal ozone exposure but not outdoor stationary site ozone (O3) was positively associated with daily asthma severity in children (1). Several of our panel studies have shown positive associations of asthma symptom severity in schoolchildren with outdoor fungal spores (1, 5-7) and pollen (7). These aeroallergens did not confound significant air pollutant effects. We also showed adverse effects on asthma symptoms from increases in daily 1-hr and 8-hr maximum PM10 (particulate matter, aerodynamic diameter < 10µm) in addition to 24-hr average PM10 (7, 8). The current averaging time for federal regulation of PM10 and PM2.5 is 24 hours. In addition, air pollutant and aeroallergen effects were notably greater among asthmatics not taking anti-inflammatory medications (7, 8).
Our initial research results on effects of peak 1-hr and 8-hr particle exposures prompted our current work funded by NIH, NIEHS. Ongoing analysis is being conducted for a study that involves intensive personal particle exposure assessments and dosimetric work in a panel of schoolchildren with asthma. Participants use electronic diaries and wear light scattering devices to provide continuous monitoring of particle exposure. We are testing the hypotheses that: 1) peak hourly exposures to particulate matter of outdoor origin will be more closely associated with acute asthmatic responses to particles than 24-hour average exposures; and 2) estimates of personal hourly particle exposures from microenvironmental models, and estimated particle dose to target zones in the respiratory tract will be more closely associated with daily asthma severity than unadjusted outdoor particle concentrations. Findings may partly explain epidemiological findings for adverse effects of regulated 24-hour average PM10 at levels below 150 mg/m3 (the U.S. National Ambient Air Quality Standard).
Another panel study was conducted involving Hispanic schoolchildren with asthma living in a region of Los Angeles County with high traffic density and high ambient air concentrations of toxic air pollutants, including volatile organic compounds (VOCs) such as benzene. We found ambient petroleum-related VOCs measured on the same person-days as exhaled breath concentrations of VOCs showed notably stronger positive associations with asthma symptoms than the breath measurements (8). VOCs included toluene, m,p-xylene, o-xylene, and benzene. Additional analyses over the 3-month daily component of this panel showed positive associations of asthma symptoms with several VOCs, US EPA principal criteria air pollutants [O3, nitrogen dioxide (NO2) sulfur dioxide (SO2) and PM10], and organic carbon and elemental carbon fractions of PM10 (EC-OC) (9). For an increase to mean concentrations, bothersome or more severe asthma symptoms were 3.0 times more likely for EC, 3.6 times more likely for OC and 1.8 times more likely for PM10. Two-pollutant regression models of EC or OC with PM10 showed little change in adjusted odds ratios from single pollutant models for EC or OC, but PM10 decreased 1.0. Organic compounds such as polycyclic aromatic hydrocarbons or other combustion products in diesel or automobile exhaust may have driven these particle associations. Taken together, these findings support the view that toxic air pollutants in the pollutant mix from traffic and industrial sources may have adverse effects on asthma.
Upcoming research funded by NIH, NIEHS involves intensive personal exposure assessments for NO2, PM10 and EC-OC. This is part of an overall interest in the Department of Epidemiology to assess the importance of air pollutants to acute asthma exacerbations in children, and to assess the relative role of toxic air pollutants to effects of regulated principal criteria air pollutants such as particle mass or NO2 (10).
Dr. Delfino and colleagues have also performed analyses on the relationship between emergency room visits to 25 hospitals for respiratory illnesses and air pollution in Montreal, Canada (11, 12). We found adverse effects on emergency room visits for respiratory illnesses among the elderly by summertime levels of ozone and particulate air pollutants well below US EPA air quality standards. Hospital admissions for asthma and other respiratory illnesses were also positively associated with ambient air pollutants (13). The overall burden of respiratory illnesses from air pollution could be much larger than that suggested by this and similar time series studies of hospital data when considering less severe clinical expressions of respiratory morbidity (symptom exacerbations, increased medication use and lung function decrements). We continue to contribute to this area of research by conducting panel studies in potentially susceptible populations.
Recent work of the Department of Epidemiology with Dr. Dan Cooper in the Department of Pediatrics, UCI and Dr. Bruce Nickerson of the Children’s Hospital of Orange County (CHOC) includes the development of research designs for the new Asthma and Chronic Lung Disease (CLD) Institute. This is a collaborative effort between CHOC and UCI Medical Center to work with the appropriate Orange County community-based resources to create comprehensive and integrated approaches to assuring access to quality care for the children of Orange County with asthma and CLD. Drs. Delfino and Carpenter in the UCI Department of Epidemiology will assist the Institute in creating an innovative, state-of-the-art database and outcome-focused tracking system to monitor care provided and health outcomes in these children. This will be accomplished through the development and implementation of a surveillance system to capture data on children ages 0-8 living in Orange County with health outcome characteristics that are associated with the development and persistent severity of asthma and CLD. This system will identify and track these children by age, race/ethnicity, geographic location, illness severity, medical home, asthma risk factors and relevant exposures, including traffic-related air pollutant exposures. This data will be used to develop prevention programs that more accurately target populations at risk. The system will conduct on-going evaluation and measurement to assess the impact of key exposures or risk factors, health promotion programs, and medical interventions.
References
1. Delfino RJ, Coate B, Zeiger RS, Seltzer JM, Street DH, Koutrakis P. Daily asthma severity in relation to personal ozone exposure and outdoor fungal spores. Am J Respir Crit Care Med, 1996; 154:633-41.
2. Liu L-J S, Delfino RJ, Koutrakis P. Ozone exposure assessment in a southern California community. Environ Health Perspect, 1997; 105:58-65.
3. Quintana PJE, Samimi BS, Kleinman MT, Liu S, Soto K, Buffalino C, Warner G, Valencia J, Francis D, Hovell MH, Delfino, RJ. Assessment of personal exposure to fine particulate matter in asthmatic children using a real-time sampler: sampler performance. J Expo Analysis Environ Epidemiol, 2000; 10:437-45.
4. Quintana PJE, Valenzia JR, Delfino, RJ, Liu L‑J S. Monitoring of 1-minute personal particulate matter exposures in relation to voice-recorded time-activity data. Environmental Research, 2001; 87:199-213.
5. Delfino RJ, Zeiger RS, Seltzer JM, Street DH, Matteucci RM, Anderson PR, Koutrakis P. The effect of outdoor fungal spore concentrations on asthma severity. Environ Health Perspect 1997; 105:622-35.
6. Delfino RJ, Zeiger RS, Seltzer JM, Street DH. Symptoms in pediatric asthmatics and air pollution: Differences in effects by symptom severity, anti-inflammatory medication use, and particulate averaging time. Environ Health Perspect, 1998; 106: 751-61.
7. Delfino RJ, Zeiger RS, Seltzer JM, Street DH, McLaren, C. Association of asthma symptoms with peak particulate air pollution and effect modification by anti-inflammatory medication use. Environ Health Perspect, 2002; 110:A607-A617.
8. Delfino RJ, Gong H Jr, Linn WS, Hu Y, Pellizzari ED. Respiratory symptoms and peak expiratory flow in children with asthma in relation to volatile organic compounds in exhaled breath and ambient air. J Expo Analysis Environ Epidemiol 2003; 13:348-63.
9. Delfino RJ, Gong H Jr, Linn WS, Hu Y, Pellizzari ED. Asthma symptoms in Hispanic children and daily ambient exposures to toxic and criteria air pollutants. Environ Health Perspect 2003; 111:647-656.
10. Delfino RJ. Epidemiological evidence for asthma and exposure to air toxics: linkages between occupational, indoor, and community air pollution research. Environ Health Perspect, 2002 110(Suppl 4):573-589.
11. Delfino RJ, Murphy AM, Burnett RT, Brook JR, Becklake MR. Effects of ozone and particulate air pollution on emergency room visits for respiratory illnesses in Montreal. Am J Respir Crit Care Med, 1997; 155:568-576.
12. Delfino RJ, Murphy-Moulton AM, Becklake MR. Emergency room visits for respiratory illnesses among the elderly in Montreal: Association with low level ozone exposure. Environ Res, 1998; 76:67-77.
13. Delfino RJ, Becklake MR, Hanley J. The relationship of urgent hospital admissions for respiratory illnesses to photochemical air pollution levels in Montreal. Environ Res, 1994; 67:1-19.
Asthma
severity and susceptibility to air pollution,
Eur Respir J 1998; 11:686-693
TJ
Hiltermann, J Stolk, SC van der Zee, B Brunekreef, CR de Bruijne, PH Fischer,
CB Ameling, PJ Sterk, PS Hiemstra, and L van Bree
Exacerbations of asthma have been associated with exposure
to ozone or particles with a 50% cut-off aerodynamic diameter of 10 microm
(PM10). We postulated in this study that the association of summertime air
pollution (i.e. ozone and PM10) with acute respiratory symptoms, medication use
and peak expiratory flow differs among patients grouped according to asthma
severity. During the summer of 1995, effects of ambient air pollution on these
parameters were studied in a panel of 60 nonsmoking patients with intermittent
to severe persistent asthma. These patients were recruited from our Pulmonary
Out-patient Clinic. Subgroup analysis was performed on the degree of
hyperresponsiveness and lung steroid use before the start of the study, as
indictors for the severity of asthma. Associations of the parameters studied
with ozone, PM10, nitrogen dioxide (NO2), sulphur dioxide (SO2) and black smoke
were evaluated using time series analysis. Several episodes with increased
summertime air pollution occurred during the 96 day study period. Eight hour
average ozone concentrations exceeded the World Health Organization (WHO) Air
Quality Guidelines (120 microg x m(-3)) on 16 occasions. Daily mean levels of
PM10 were moderately elevated (range 16-98 microg x m(-3)). Levels of the other
measured pollutants were low. There was a consistent, positive association of
the prevalence of shortness of breath (maximal relative risk (RRmax) 1.18) with
ozone, PM10, black smoke and NO2. In addition, bronchodilator use was
associated with both ozone and PM10 levels (RRmax 1.16). Stratification by
airway hyperresponsiveness and steroid use did not affect the magnitude of the
observed associations. No associations with peak expiratory flow measurements
were found. We conclude that the severity of asthma is not an indicator for the
sensitivity to air pollution.
Relationship Between PM10 Concentrations and Asthma Patients
in Metropolitan Areas in Korea Using Spatial and Time-Trend Analysis, Yi, O; Park, A; Huh, J; Kim, H; Epidemiology:
November 2008 - Volume 19 - Issue 6
- p S249
Analysis using local emission resulted in 11 clusters with the regional characteristics and analysis with long-range transport resulted in 4 clusters where no regional characteristics remained. The number of patients with asthma for 10 days standardized by the population size within clusters had the dose-response relationship with the PM10 concentration in clusters.
Results from this study suggests that control of transport-in pollutants is as important as the local emission control in order to reduce the level of PM10 concentrations.
Lokman Hakan Tecer a; Omar Alagha b;
Ferhat Karaca b; G
rdal
Tuncel c; Nilufer Eldes d , Journal of Toxicology and
Environmental Health, Part A, Volume 71, Issue 8 January 2008 , pages 512 – 520
Epidemiological studies reported adverse effects of air pollution on the prevalence of respiratory diseases in children. The purpose of this study was to examine the association between air pollution and admissions for asthma and other respiratory diseases among children who were younger than 15 yr of age. The study used data on respiratory hospital admissions and air pollutant concentrations, including thoracic particulate matter (PM10), fine (PM2.5), and coarse (PM10-2.5) particulate matter in Zonguldak, Turkey. A bidirectional case-crossover design was used to calculate odds ratios for the admissions adjusted for daily meteorological parameters. Significant increases were observed for hospital admissions in children for asthma, allergic rhinitis (AR), and upper (UPRD) and lower (LWRD) respiratory diseases. All fraction of PM in children showed significant positive associations with asthma admissions. The highest association noted was 18% rise in asthma admissions correlated with a 10-μg/m3 increase in PM10-2.5 on the same day of admissions. The adjusted odds ratios for exposure to PM2.5 with an increment of 10 μg/m3 were 1.15 and 1.21 for asthma and allergic rhinitis with asthma, respectively. PM10 exerted significant effects on hospital admissions for all outcomes, including asthma, AR, UPRD, and LWRD. Our study suggested a greater effect of fine and coarse PM on asthma hospital admissions compared with PM10 in children.
Reductions in mortality following improvements in air quality
were documented by several studies, and our group found, in an earlier
analysis, that decreasing particulate levels attenuate lung function
decline in adults. Methods: The
present analysis includes 7,019 subjects who underwent detailed
baseline examinations in 1991 and a follow-up interview in 2002.
Each subject was assigned model-based estimates of average PM10
during the 12 months preceding each health assessment and the
difference was used as the exposure variable of interest (
PM10).
Analyses were stratified by symptom status at baseline and
associations between
PM10
and change in symptom status during follow-up were adjusted for
important baseline characteristics, smoking status at follow-up, and
season. We then estimated adjusted odds ratios for symptoms at
follow-up and numbers of symptomatic cases prevented due to the
observed reductions in PM10.
Measurements and Main Results: Residential exposure to PM10 was lower in 2002 than in 1991 (mean decline 6.2 µg/m3; SD = 3.9 µg/m3). Estimated benefits (per 10,000 persons) attributable to the observed changes in PM10-levels were: 259 (95% confidence interval [CI]: 102–416) fewer subjects with regular cough, 179 (95% CI, 30–328) fewer subjects with chronic cough or phlegm and 137 (95% CI, 9–266) fewer subjects with wheezing and breathlessness.
Conclusions: Reductions in particle levels in Switzerland over the 11-year follow-up period had a beneficial effect on respiratory symptoms among adults.
STUDIES have demonstrated an association between respiratory disease and suspended particulate pollution in ambient air. [1-13] It has been reported recently that even moderately elevated concentrations of particulate pollution may result in reductions in children's pulmonary function [14-15] and in increased risk for bronchitis and other respiratory illnesses. [16-17] Suspended sulfate and nitrate particles, which may contain sulfuric and nitric acids, are of particular concern. [18-31] Fine particulate pollution can damage human health because it often contains toxic substances, e.g., acid sulfates and trace metals, and because it sometimes evades defense mechanisms of the respiratory system. [31-35]
Two recent studies evaluate the impact of air pollution on the respiratory health of persons living in Utah Valley. The first study [36] assessed the association between respiratory hospital admissions and particulate pollution with an aerodynamic diameter equal to or less that a nominal 10 micrometers ([PM.sub.10]). [32] The valley's major emitter of [PM.sub.10], a local steel mill, operated intermittently during the study period. Strong associations between respiratory hospital admissions, [PM.sub.10] pollution, and the operation of the local steel mill were observed. The second study [37] compared age-adjusted death rates for malignant and nonmalignant respiratory disease across Utah, Salt Lake, and Cache counties in Utah. Various factors that might cause differences in respiratory disease, including smoking and air pollution, were evaluated. A strikingly large percentage (30-40%) of respiratory cancer and nonmalignant respiratory disease deaths in Utah County were estimated as being attributable to air pollution.
PM10 and asthma medication in schoolchildren. Mary Ellen Gordian; Askar H Choudhury; Arch. Environ. Health, Jan 2003
The authors found that the use of asthma medication among elementary schoolchildren was associated with particulate pollution (particulate matter < 10 microm in aerodynamic diameter [PM10]) in a locale where PM10 consisted primarily of coarse fraction material derived from road sanding and reentrained volcanic ash. School nurses' records in 12 neighborhood schools located close to an ambient air monitoring station were abstracted, and the numbers of oral and inhaled doses of asthma medication given daily over a period of 2.5 yr were calculated. Time-series regression models, adjusted for autocorrelation, were developed, with temperature, time trend, day of the week, and month as additional variables. Regression models were estimated, and a lagged moving average of PM10 for 7, 14, 21, and 28 days was used. All models showed positive and significant coefficients for PM10 during periods when asthma medication was administered to the schoolchildren. However, the 21-day moving average was the best fit to the model.
Many time-series studies have shown positive associations between air pollutants and asthma morbidity. However, few studies have included pollen as a potential confounder when examining this relationship.
This study analysed the short-term association between air pollutants (sulphur dioxide (SO2), particles measured with a median aerodynamic diameter of <10 µm (PM10), nitrogen dioxide (NO2) and ozone (O3)) and asthma emergency room admissions in Madrid, Spain, in 1995–1998, adjusting for four types of pollen with allergenic potential (Olea europaea, Plantago sp., Poaceae and Urticaceae). Data were analysed using autoregressive Poisson regression and generalised additive models (GAM).
The strongest associations were observed at 1 day lag for O3, and 3 days lag for the remaining pollutants. Using Poisson regression, a single-pollutant model showed that a 10-µg·m–3 rise in pollutant level led to relative risks of: 1.039 for PM10; 1.029 for SO2; 1.033 for NO2; and 1.045 for O3. Adjustment for the different types of pollen led to no substantial variation in these associations. In the multipollutant models for cold-season pollutants (including PM10, SO2 and the four types of pollen) and photochemical pollutants (including NO2, O3 and the four types of pollen) the associations for PM10, NO2 and O3 held, but no relationship with SO2 was evident. GAM analysis yielded the same results, both in terms of lags and of quantification of the effect for all pollutants.
In conclusion, the usual air
pollution levels in Madrid were associated with an increase in
asthma emergency room admissions, and this association remained
controlling for the presence of ambient pollen.
Effect of PM10 pollution in Bangkok on children with and without asthma, Pediatr Pulmonol. 2004; 37:187-192. Aroonwan Preutthipan, MD, FCCP 1 *, Umaporn Udomsubpayakul, MS 2, Thitida Chaisupamongkollarp, MS 3, Prapat Pentamwa, MSc 4
T his
study aimed to investigate the effects of PM10 concentrations
exceeding the Thai national standard (24-hr average, >120
g/m3)
on daily reported respiratory symptoms and peak expiratory flow rate (PEFR) of
schoolchildren with and without asthma in Bangkok. The 93 asthmatic and 40
nonasthmatic schoolchildren were randomly recruited from a school located in a
highly congested traffic area. Daily respiratory symptoms and PEFR of each
child were evaluated and recorded in the diary for 31 successive school days.
During the study period, 24-hr average PM10 levels ranged between
46-201
g/m3.
PM10 levels exceeded 120
g/m3
for 14 days. We found that when PM10 levels were >120
g/m3,
the daily reported nasal irritation of asthmatic children was significantly
higher than when PM10 levels were
120
g/m3.
In addition, when PM10 levels were >120
g/m3,
nonasthmatic children had a
significantly higher daily reported combination of any respiratory symptoms.
PEFR did not change with different ambient PM10 levels in both
groups. This study suggests that elevated
levels of PM10 concentrations in Bangkok affect respiratory symptoms
of schoolchildren with and without asthma.
Asthma and PM10
Kenneth Donaldson,
1,2
M Ian Gilmour,3 and William MacNee2
Respir Res. 2000; 1(1): 12–15.
PM10 (the mass of particles present in the air having a 50% cutoff for particles with an aerodynamic diameter of 10 μm) is the standard measure of particulate air pollution used worldwide. Epidemiological studies suggest that asthma symptoms can be worsened by increases in the levels of PM10. Epidemiological evidence at present indicates that PM10 increases do not raise the chances of initial sensitisation and induction of disease, although further research is warranted. PM10 is a complex mixture of particle types and has many components and there is no general agreement regarding which component(s) could lead to exacerbations of asthma. However pro-inflammatory effects of transition metals, hydrocarbons, ultrafine particles and endotoxin, all present to varying degrees in PM10, could be important. An understanding of the role of the different components of PM10 in exacerbating asthma is essential before proper risk assessment can be undertaken leading to advice on risk management for the many asthmatics who are exposed to air pollution particles.