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Atmospheric Environment 45 (2011) 1781e1785

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Atmospheric Environment

journal homepage: www.elsevier .com/locate/atmosenv

Review

Air pollution exposure: Who is at high risk?

Ronit Peled*

Department of Health Systems Management, Faculty of Health Sciences, Ben Gurion University of the Negev, Beer Sheva 84105, Israel

a r t i c l e i n f o

Article history:Received 24 May 2010Received in revised form2 January 2011Accepted 3 January 2011

Keywords:Air pollutionPopulation at risk

* Tel.: þ972 507 535557; fax: þ972 8 6726290.E-mail address: ronitpeled@yahoo.com.

1352-2310/$ e see front matter � 2011 Elsevier Ltd.doi:10.1016/j.atmosenv.2011.01.001

a b s t r a c t

This article reviews the sub-population groups who are at high risk and first to be harmed by airpollution coming from anthropogenic combustions. Epidemiological studies from the last few decadescontributed to the understanding of the different levels of susceptibility to air pollution. Older peopleand young infants, people who suffer from allergies, pulmonary and heart diseases, pregnant women andnewborn babies, and deprived populations that suffer from low socio-economic status have all beendescribed as populations at risk. A better understanding of the role of air pollution on large as well asspecific populations’ health, will promote a better protection policy.

� 2011 Elsevier Ltd. All rights reserved.

1. Introduction

Air pollution policy is basically informed to protect publichealth. National guidelines and air quality standards are set for theentire population.

Typically, the same relative risks are applied to all individuals“at-risk” and baseline rates of mortality, morbidity, and health careuse are assumed to be uniform across large geographic areas (oftennational averages) (Levy et al., 2002). For example: the AmericanEnvironmental Protection Agency estimates that meeting existingPM2.5 standards will prevent at least 15,000 premature deaths,75,000 cases of chronic bronchitis, 10,000 hospital admissions forrespiratory and cardiovascular disease, hundreds of thousands ofoccurrences of aggravated asthma, and 3.1 million days whenpeople miss work because they are suffering from symptomsrelated to particle pollution exposure (EPA, 2005). However, studiesfrom the last decade pointed out different levels of risk andsusceptibility across subpopulations. The definition of sub-pop-ulation and susceptible groups is important for research and policydecisions, especially when guidelines and pollution standards areset. These groups include: newborns, young infants, toddlers, theelderly, people who suffer from respiratory, cardiovascular andother diseases, people who suffer from medical conditions such asallergies and pregnancy and deprived populations.

The objective of this article is to describe and review the mainsub-population groups who were identified as susceptible to airpollution mainly coming from anthropogenic combustions: Sox;

All rights reserved.

Nox; CO and other sources: Fine Particles and O3. Medline was usedto review the literature (PubMed).

2. Age

2.1. Older people (65þ years of age)

Not many studies have focused on the elderly population, whichis a fast-growing segment in both developed and developingcountries. The elderly are more susceptible to harm from toxicsubstances because of their depressed immune systems, existingdiseases, and the accumulation of toxic agents in their bodies (Sunand Gu, 2008). Extreme air pollution events occurred in the earlytwentieth century in Meuse River Valley, France, in 1930; Donora,Pennsylvania, in October 1948; and in London between the 5th andthe 9th of December 1952, led to the first construction of an asso-ciation between air pollution and health. In these events the first tobe harmed were the sick and the old people.

Since then, studies from all over the world have reported greaterrisks of death from particulate matter (PM) in the population >65-years-of-age in six cities (Dockery et al., 1993): Philadelphia, PA, USA(Schwartz and Dockery, 1992), Cincinnati, OH, USA (Schwartz, 1994),Amsterdam, The Netherlands (Verhoeff et al., 1996), Mexico City,Mexico (Borja-Aburto et al., 1998), Montreal, Quebec, Canada(Goldberg et al., 2001), and Sao Paulo, Brazil (Gouveia and Fletcher,2000). In a study from Rotterdam, The Netherlands (Hoek et al.,1997), Total Suspended Particles (TSP) and especially O3 RelativeRateswere substantiallygreater fordeaths inadults>78-years-of-age.

When looking at epidemiologic studies linking air pollution andnumber of deaths, one should be aware of the “harvesting effect”,also known as mortality displacement. This effect appears where

R. Peled / Atmospheric Environment 45 (2011) 1781e17851782

the people whose deaths are attributed to air pollution and wereabout to die within a few days anyway. In this case, increases inmortality rates following high levels of air pollution were matchedalmost immediately by a corresponding reduction in mortalityrates, indicating that air pollution is killing primarily the frail andthose whose life expectancy was already quite short. Also, ifmortality rates afterwards almost unchanged, suggesting that airpollution is killing individuals who might not otherwise have livedsome considerable time (Maddison, 2006). This possible effectshould be taken into account when establishing policy and settingthresholds.

If not looking at death rates, air pollution epidemiology studieslooked at parameters representing morbidity such as: reduction inlung functions, hospital admissions due to asthma exacerbationand related attacks, stroke, chronic obstructive pulmonary disease(COPD), type 2 diabetes and cardiovascular symptoms. A studyconducted in Finland between 1998 and 2004 suggested an asso-ciation between hospital admissions for arrhythmia in people overthe age of 65 and traffic-related ultra-fine particles. Otherwise fewassociations were observed between various sizes and types ofparticles and cardiovascular admissions or mortality. In contrast,most particle fractions had positive associations with admissionsfor pneumonia, chronic asthma, and COPD. The strongest and mostconsistent associations were described between accumulationmode particles (3.1%; 95% confidence interval (CI):0.43e5.8) andpneumonia over a 5-day mean (3.8%; 95% CI:1.3e6.3), asthma andCOPD at lag 0 (Halonen et al., 2009).

A cross sectional study from West Germany pointed out anassociation between traffic-related air pollution and incident type 2diabetes amongelderlywomen. The authors suggest that sub-clinicalinflammation may be a mechanism linking air pollution with type 2diabetes (Krämer et al., 2010). Furthermore, it remains unclearwhether elderly people are more sensitive to specific components inthe air pollution mixture, although some of the studies suggest thatparticulate air pollution is most consistently associated with higherRelative Risk in the elderly (Fischer et al., 2003).

2.2. Young infants and children

The periods of fetal and child development arguably representthe stages of greatest vulnerability to the dual impacts of fossil fuelcombustion. Air pollution as fine particles, polycyclic aromatichydrocarbons (PAHs), sulfur and nitrogen oxides, benzene, andmercury emitted by coal-burning power plants, and diesel andgasoline-powered vehicles, has been variously linked to infantmortality, lower birth weight, deficits in lung function, respiratorysymptoms, and childhood asthma and leukemia (Bobak and Leon,1992; Lee et al., 2003; Gauderman et al., 2004; Peled et al., 2004;Miller et al., 2004; Weng et al., 2009). The lungs of young chil-dren are not completely formed; from birth to four-years-of-agetheir lungs undergo considerable development that culminates atsix-years-of-age. At the same time the child’s immune system,immature at birth, is also beginning to develop (Schwartz, 2004). Inaddition, children breathe 50% more air per kg body weight thanadults and spend more time outdoors, which makes their exposuregreater. Moreover, damaging childhood development has lifelongconsequences. This is why exposure to air pollution in childhoodincreases the risk of chronic respiratory illness and cardiovasculardiseases in adulthood (Shea, 2003).

3. Adults and children with asthma and other respiratorydiseases

Asthma is a very common chronic illness, with prevalenceestimates of approximately 8% of the United States population

(National health statistics, 2002), and the second most commoncause of hospitalizations in children (Global Initiative, 2004).Asthma is a lung disease manifested symptomatically with airwayobstruction that is reversible (although incompletely in somepatients) either spontaneously or with treatment. Airway inflam-mation and airway hyper-responsiveness are related to the disease(National Heart Lung and Blood,1992). Inflammation of the airwaysis the common finding in all asthma patients. This inflammation isproduced by allergies, viral respiratory infections, and airborneirritants among other causes. This airway inflammation can causescarring if it goes on for a long period of time (Childhood AsthmaOverview). Thus, most asthma conditions are attributed to envi-ronmental exposures such as allergens, secondhand smoke, andoutdoor air pollution. Outdoor pollutants well known to triggerasthma attacks include ozone, particulate matter, nitrogen dioxide,and sulfur dioxide (Delfino et al., 2009). Exposure to particulatematter and volatile organic compounds arising from petrochemicalplants were associated with worse respiratory health in childrenfrom La Plata, Argentina (Wichmann et al., 2008) and Israel (Peledet al., 2005). Results from a French study suggested that ozone orrelated ambient pollutants may up regulated total IgE serum levelsamong asthmatic adults (Rage et al., 2009a,b). In Switzerland anassociation between asthma severity and air pollution wasobserved-ozone in particular, supported the hypothesis that airpollution at levels below current standards increases asthmaseverity (Rage et al., 2009a,b). Chronic obstructive pulmonarydisease (COPD) is a progressive disease that makes it hard tobreathe, getting worse over time and attacks adults. COPD cancause coughing that produces large amounts of mucus, wheezing,shortness of breath, chest tightness, and other symptoms. Cigarettesmoking is the leading cause of COPD. Most people who have COPDare current or past smokers. Long-term exposure to other lungirritants, such as air pollution, chemical fumes, or dust, also maycontribute to COPD (National Heart Lung and Blood, 1992). COPDwas described as associated with traffic-related air pollution(Lindgren et al., 2009). This indicates that this source of air pollu-tion has both long-term and short-term effects on chronic respi-ratory disease in adults and children, even in regions with overalllow levels of pollution. Fine particles pollution was associated witha reduction in lung function in childrenwith asthma living near twopower plants in Israel (Peled et al., 2005). In this time series studya panel of school children diagnosed as having asthma performeda self-examination for lung function twice a day and recordeda diary along with daily air pollution and meteorological conditionmeasurements. Part of the association was found to be due to aninteraction between air pollution seasonality and meteorologicalconditions, mainly temperature.

The overall evidence consistency indicated the susceptibility ofchildren and adults with asthma and other respiratory diseases.These sick people are vulnerable to air pollution of all kinds atsignificantly less than traditional thresholds and are the first to beharmed.

4. Adults with cardiovascular diseases

Numerous studies suggest that long-term or short-term expo-sure to higher levels of outdoor air pollution, particularly particu-late matter, increases risk of cardiovascular death andcardiovascular disease (Committee on the Medical Effects, 2006;Brook et al., 2004; Miller et al., 2007; Pope et al., 2004a,b). Thehypothesis is that inhalation of fine particles provokes inflamma-tion in the lung, causing the release of inflammatory mediators intothe bloodstream that may influence homeostasis or accelerateatherosclerosis. This is mademore plausible by the observation thatchronic low-grade inflammation is a risk factor for cardiovascular

R. Peled / Atmospheric Environment 45 (2011) 1781e1785 1783

disease (Forbes et al., 2009). Experimental studies in small numbersof human volunteers have shown systemic inflammation (Salviet al., 1999) or changes in heart rate variability (HRV) resultingfrom exposure to fine particles (Pope et al., 2004a,b) or asa response to inhaling environmental tobacco smoke (Pope et al.,2001). A study conducted by Pope and colleagues in the USAanalyzed hospitalization data of patients with heart failure (HF)who lived in a well-defined area with substantial temporal vari-ability in fine particles, in addition to concentrations due to denselypopulated mountain valley topography and frequent temperatureinversions. It was hypothesized that elevated PM concentrationswill be associated with increased risk of HF hospitalization. Also,because hospitalization follows onset of symptoms, which likelyfollow a period of cumulative exposure, a distributed lag structurerelating exposure to hospitalization of a few days or more washypothesized. This study indicated that lagged cumulative expo-sures to PM2.5 of one to several weeks was significantly associatedwith increased risk of HF exacerbations, as represented by hospi-talization with a primary discharge diagnosis of HF (Pope et al.,2008). These studies and others suggested that exposure to airpollution may exacerbate HF and other cardiovascular conditionsby triggering decompensation through effects of air pollution,particularly fine particles, on myocardial ischemia, cardiac auto-nomic function, and/or arrhythmic effects.

5. Health conditions

5.1. Allergy

Reviews of the effects of air pollution on allergies haveconcluded that pollutants likely exacerbate effects of allergensamong those with existing susceptibility, rather than initiatingallergies among people without existing allergies (Bartra et al.,2007; D’Amato et al., 2005; Von Mutius, 2000).

Possible rationales for the associations between components ofair pollution, allergens, and allergic response include the effect ofthe pollutants on the potency of the allergens and the increasedsusceptibility of the subjects via an inflammatory effect on theairways, in addition to increased airway reactivity, or increasedbronchial responsiveness.

An interesting study from California looked for an associationbetween pre-natal and early-life exposures to outdoor air pollut-ants with allergic sensitization. Allergic sensitization was ascer-tained by skin-prick tests to 14 allergens in addition to pre-nataland early-life exposure assessment to ozone, nitrogen dioxide,carbon monoxide, and fine particulate matter. The results sug-gested that exposure to traffic-related pollutants, mainly carbonmonoxide, during pregnancy may increase the risk of sensitizationto outdoor allergens in asthmatic children (Mortimer et al., 2008).

In a very large scale study, Parker and her colleagues (Parkeret al., 2008) examined whether air pollutants were associatedwith childhood respiratory allergies in the United States. Dataabout 70,000 children from the 1999e2005 National HealthInterview Survey, in addition to data of 40,000e60,000 ambientpollution measurements within 20 miles of the child’s residentialblock, gathered from the U.S. Environmental Protection Agencywere analyzed. The results show increased respiratory allergy/hayfever associated with increased summer O3 levels (adjusted oddsratio (AOR) per 10 ppb ¼ 1.20; 95% CI:1.15e1.26) and increasedPM2.5 (AOR per 10 mg m�3 ¼ 1.23; 95% CI:1.10e1.38). These asso-ciations persisted after stratification by urbanerural status, inclu-sion of multiple pollutants, and definition of exposures. Noassociations between the other pollutants and the reported respi-ratory allergy/hay fever were apparent.

A number of clinically important allergens coming from indoorsources should be taken into consideration while looking for pop-ulations at risk for air pollution. These are house-dust mites, pets,cockroaches, fungi, and insects. The multicolored Asian Lady Beetlehas recently been identified as a seasonal indoor allergen source inplaces where this insect was imported (Nakazawa et al., 2007).

5.2. Pregnant women and newborns

The effect of ambient air pollution on birth outcomes e birthweight and pre-natal morbidity e is of great concern for publichealth. Undesired birth outcomes has an impact on newborns’survival, children’s development, and chronic diseases. It isbelieved that the association between air pollution and adversebirth outcomes arises as a result of the phenomenon of “epigeneticprogramming”, which involves persisting changes in structure andfunction caused by environmental factors during critical andvulnerable periods early development (Barker, 2004; Phillips,2000).

In a study conducted in Poland (Jedrychowski et al., 2009), 481women 18e35-years-of-age, who claimed to be non-smokers, withsingleton pregnancies, without illicit drug use or HIV infection, freefrom chronic diseases, were recruited, giving birth between 37 and43 weeks of gestation. Pre-natal personal exposure to fine particlese PM2.5 e was measured using personal monitors. Each newbornwas measured at birth for weight, length, and head circumference.This study suggested that after controlling for potentialconfounders (maternal education, gestational age, parity, maternalheight and pre-pregnancy weight, sex of infant, pre-natal envi-ronmental tobacco smoke, and season of birth), birth outcomeswere associated negatively with the level of pre-natal PM2.5exposure. Overall average increase in gestational period of pre-natal exposure to fine particles by about 30 mg m3, i.e., from 25thpercentile (23.4 mg m3) to 75th percentile (53.1 mg m3) broughtabout an average birth weight deficit of 97.2 g (95% CI: �201, �6.6)and length at birth of 0.7 cm (95% CI: �1.36, �0.04). The corre-sponding exposure led to a birth weight deficit inmale newborns of189 g (95% CI: �34.2, �343) in comparison to 17 g in femalenewborns; the deficit of length at birth in male infants amounted to1.1 cm (95% CI: �0.11, �2.04). A study from Atlanta, Georgia(Strickland et al., 2009) looked for an association between exposureto ultra-fine particles during 3e7 weeks of pregnancy and the riskof cardiovascular malformations among a cohort of pregnanciesreaching at least 20 weeks of gestation between 1986 and 2003.The results show a statistically significant association only betweenPM10 and patent ductus arteriosus (for an interquartile rangeincrease in PM10 levels, risk ratio ¼ 1.60, 95% CI:1.11e2.31).

Birth weight is an important variable for measuring perinataloutcomes. Birth weight depends on maternal, placental, and fetalfactors, all of them influenced by environmental sources. Low birthweight (LBW) is considered when the baby is less than 2500 g atbirth; it is themost important predictor of neonatal mortality and isa significant determinant of post-neonatal mortality andmorbidity.

Few studies attempted to investigate the role of air pollution inLBW.Most of them emphasized the importance of exposure in earlygestation periods. A study from Seoul, Korea (Lee et al., 2003),evaluated the relationship between LBW and exposure in 2e5months of pregnancy to carbon monoxide (CO), PM10, sulfurdioxide (SO2), and nitrogen dioxide (NO2). This study has suggestedthat exposure to CO, PM10, SO2, and NO2 during early to mid-pregnancy contributes to the risk of LBW.

A recently published study from Switzerland (Latzin et al., 2009)describes an association between pre-natal exposure to air pollu-tion and reduction in lung function among healthy full-termnewborns. In a prospective birth cohort of 241 neonates, tidal

Table 1Selected health factors, air pollution concentrations and population at high risk.

Pollutant Health Effect Concentrations Population at Risk Reference

Inhaled Particles Mortality 18.2e46.5 mg m�3 Adults 25e74 y Dockery et al. (1993)Fine Particles 11.0e29.6 mg m�3

Sulfat Particles 4.8e12.8 mg m�3

PM2.5 Hospital Admissions forCardio-Respiratory Diseases

1.1e69.5 mg m�3 Adults 65þ y Halonen et al. (2009)NO2 3.4e96.4 mg m�3

PM10 Type 2 Diabetes 44.0e54.1 mg m�3 Women Mean Age 54 y Kramer et al. (2010)NO2 23.3e48.2 mg m�3

NO2 Growth of Lung Function 5.0e38.0 ppb Children (Mean Age 10 y) Gauderman et al. (2004)NO2 Asthma Severity Mean: 40.2 � 14.7 mg m�3 Adults Rage et al. (2009a,b)SO2 Mean: 21.3 � 8.6 mg m�3

O3 Mean: 60.5 � 19.4 mg m�3

PM2.5 Heart Failure Hospitalizations Mean: 10.6 � 9.9; 11.9 � 11.8 mg m�3 Adults 67 þ 15 y Pope et al. (2008)

R. Peled / Atmospheric Environment 45 (2011) 1781e17851784

breathing, lung volume, ventilation inhomogeneity, and exhalednitric oxide (eNO) were measured during unsedated sleep at age 5weeks. Maternal exposure to particles (PM), nitrogen dioxide(NO2), and ozone (O3), and distance from major roads were alsoestimated during pregnancy. The results of this study show thatminute ventilation was greater in infants with higher pre-natalPM10 exposure (24.9 mL � min�1 per mg � m�3). The eNO wasincreased in infants with greater pre-natal NO2 exposure(0.98 ppb per mg � m�3). Post-natal exposure to air pollution didnot modify these findings. No association was found for pre-natalexposure to O3 and lung function parameters. In summary, thisstudy suggests that pre-natal exposure to air pollution might beassociated with greater respiratory need and airway inflammationin newborns. Such alterations during early lung development maybe important regarding long-term respiratory morbidity.

6. Deprived population e low socio economic status

Deprived populations are at risk for various health determinantslinked to adverse birth outcomes, lack of access to health care andempowerment, level of stress and violence, and likelihood ofexposure to environmental hazards including air pollution (Zekaet al., 2008). In Massachusetts, USA, researchers looked at linksbetween exposure to No2 mainly coming from traffic sources andsocio-economic status (SES) using a geographic information system(GIS). NO2 concentrations were significantly negatively associatedwith median household income, and positively associated withpoverty, crowding, and low educational attainment rates aftercontrolling for spatial autocorrelation. A Study from Hong Kongfound out that air pollution mortality effects for SO2 were strongerin highly Social deprived areas (Social Deprivation Index ¼ SDI)compared low SDI. In this study, in addition to SO2 the authorsfound that those residing in high SDI areas had higher excess risk ofdeath also associated with NO2, particularly for cardiovasculardisease, than those in low SDI areas. The scientists of this studysuggest a possible explanation that lies in the fact that sociallydeprived subgroups are more likely to have poorer health care andnutrition and other increased health risks, resulting in increasedsusceptibility to the adverse effects of air pollution (Wong et al.,2008).

The biologic mechanisms underlying the health effects of airpollution can be explained in terms of oxidative stress and immunesystem damage after both long- and short-term exposures. Thereare two main hypotheses regarding the possible effect of theinteractions between air pollution and socio-economic status onhealth. First, people of lower socio-economic status are more likelyto live and work in places with more toxic pollution. An alternativehypothesis is that because of inadequate access to medical care,lack of material resources, poorer nutrition, and higher smoking

prevalence, those of lower socio-economic status may be moresusceptible to the adverse effects of air pollution than those inhigher socio-economic groups (O’Neill, 2003).

7. To summarize

The characterization and definition of air pollution at-risksubpopulations can contribute both to risk assessment andmanagement and to exposure assessment and environmentalepidemiological studies. However, studies in air pollution epide-miology are highly challenging. One of the great challenges lie inthe fact that Subjects may substantially differ by the degree of theirpersonal exposure. Traditionally, air pollution is measured by fixedmonitoring stations. Data from these stations represent the pollu-tion of an area inwhich they are located and not necessarily areas inwhich the study subjects reside. Therefore, ambient air pollutionmeasurement data do not adequately represent personal exposureand the exposure differs between study participants.

This article did not discuss in depth the health risk as associatedwith pollution concentrations. However, Table 1 summarizesselected pollutants and their concentrations as they were found tobe associated with health effects.

Yet, knowing who are at risk to be harmed from air pollution ingeneral and from specific components and or sources can increaseour awareness and strengthen our efforts to reduce emissions,change exposure policy, and set guidelines for public healthprotection.

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