Air Pollution: Health and Environmental Impacts

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Air Pollutants Exposure and Health Effects during the MILAGRO– MCMA2006 Campaign Horacio Tovalin, Olf Herbarth, Martha P. SierraVargas, Bo Strandberg, Salvador Blanco, Libia Vega, Constantinos Sioutas, Juan J. Hicks, Rubén Marroquín, Gustavo Acosta, Marco Guarneros, Vicente Hernández, Elizabeth EstradaMuñiz, Ivonne M. Olivares, Dora A. Pérez, Yessica Torres-Ramos, Frank Ulrich, Robyn Hudson, Ernesto Reyes, Tracy Rodríguez, Guillermo Elizondo, and Eliseo Cantellano

Contents 7.1 7.2 7.3 7.4

Introduction...................................................................................................204 Air Pollution-Related Health Effects in MCMA...........................................204 High-Risk Populations...................................................................................206 The MCMA-2006 Campaign........................................................................208 7.4.1 Ozone.................................................................................................209 7.4.2 PM2.5..................................................................................................209 7.4.3 UF Particles....................................................................................... 211 7.4.4 Endotoxins......................................................................................... 213 7.4.5 Fungi.................................................................................................. 213 7.4.6 VOCs................................................................................................. 214 7.4.7 Carbon Monoxide.............................................................................. 215 7.4.8 Respiratory and Olfactory Condition................................................ 215 7.4.9 Oxidative Stress in Children.............................................................. 216 7.4.10 Oxidative Stress in Adults................................................................. 216 7.4.11 Cytokines........................................................................................... 218 7.5 Conclusions....................................................................................................220 Acknowledgments................................................................................................... 222 References............................................................................................................... 223 203

204

Air Pollution

7.1 Introduction Mexico City Metropolitan Area (MCMA) is one of the most densely populated cities in the world, with 18 million people according to the 2000 census (INEGI, 2001). MCMA is at an altitude of 2240 m above sea level, surrounded by mountains on the south, west, and east. Air pollution driven by local emissions can affect large areas within closed valleys, where restricted air movement concentrates the pollutants. Due to the altitude and latitude, MCMA receives intense solar radiation, a condition that added to a less efficient combustion promotes the photochemical formation of secondary pollutants such as ozone and particulate matter (PM) (Molina and Molina, 2002). In Mexico City, the concentrations of some of the criteria air pollutants have declined during the last decade. However, ozone and PM concentration remain above the Mexican standard for many days in certain city zones. Forty percent of the ozone (O3) measurements in 2006 were above the 0.11 ppm 1-hour standard and 50% were above the 0.08 ppm 8-hour standard. Twenty percent of the time, PM smaller than 10 µm (PM10) concentrations was above the 120 µg/m3 24-hour standard and more than 4 million of children lived in areas where PM smaller than 2.5 µm (PM2.5) concentrations was above the 15 µg/m3 annual standard (SMA, 2007). Furthermore, some substances emitted by mobile sources are recognized as carcinogenic or genotoxic, such as benzene, 1,3-butadiene, formaldehyde, cadmium, and others (IARC, 2009); they are not monitored regularly, but have high concentrations outdoors and indoors (SerranoTrespalacios et al., 2004). Observations from the intensive MCMA-2003 Campaign showed that MCMA motor vehicles produce high levels of primary PM, particle-bound polycyclic aromatic hydrocarbons (PAHs), and a wide range of air toxics, including formaldehyde, acetaldehyde, benzene, toluene, and xylenes (Molina et al., 2007).

7.2 Air pollution-related health effects in MCMA Cohen et al. (2005) reported that air pollution in developed and developing countries causes about 3% of mortality from cardiopulmonary disease, about 5% of mortality from cancer of the trachea, bronchus, and lung, and about 1% of mortality worldwide from acute respiratory infections in children younger than 5 years. These effects represent about 0.8 million (1.2%) premature deaths and 6.4 million (0.5%) years of life lost. Other epidemiological studies have demonstrated health impacts for total suspended matter (TSP), PM10 and PM2.5, the latter being the most suitable measure for health effects (Téllez-Rojo et al., 2000). Furthermore, newer epidemiological studies indicate the importance of smaller than 1-µm fine particles, including so-called ultrafine (UF) particles ( outdoor > personal levels. Depending on sampling sites, the concentrations ranged typically from 0.3–4 µg/m3 and 2–10 µg/m3 for 1,3-butadiene and benzene (Figure 7.8), respectively. A comparison between indoor and outdoor levels showed higher indoor concentrations, possibly due to cigarette smoke in those homes. In general, the personal sample levels reflect those obtained by corresponding stationary indoor or outdoor sampling results. VOC levels in the MCMA were higher than those at other urban sites (Rehwagen et al., 2003). It is important to note that MCMA VOC emissions apparently influence VOC levels at suburban (T1) and semirural (T2) sites and their surrounding areas. This MCMA influence is supported by the observation that T1 local VOC emissions represent less than 0.04% of the State of Mexico’s urban counties since it has only seven industrial/commercial units reported in a recent emissions inventory (SMAEM, 2004). There is no VOC emission inventory available for T2, but it can be expected that local VOC emissions at that site are low.

Site Iztapalapa-T0 Tecamac-T1 San Pedro-T1

μg/m3

30

20

Figure 7.7 VOC indoor levels by site (µg/m3).

TECE

TCE

StyTol

oXylene

MTCP

mpXilence

ETBZ

MCHX

Chiclohexane

0

Benzene

10

215

Air Pollutants Exposure and Health Effects –99.136

–98.972

–98.808

Symbols (μg/m3)

T2 ZAPOTLÁN DE JUÁREZ EDO. DE HIDALGO

0.0000 0.0001 – 2.9232

19.883

–99.299

19.883

–99.463

2.9233 – 4.7385 4.7386 – 9.6091

19.731

19.731

9.6092 – 18.9552

19.427

19.427

19.579

19.579

T1 TECÁMAC EDO. DE MÉXICO

T0 IZTAPALAPA D.F.

–99.463

–99.299

–99.136

0 0 025 0 05

–98.972

01

0 15

–98.808

02

Km

Figure 7.8â•… Benzene levels at homes indoors and outdoors, and personal exposure by site (µg/m3).

7.4.7â•…Carbon Monoxide CO levels for each microenvironment, as well as personal exposure levels, were higher at the urban sites. For T1 and T0 homes, outdoor CO concentrations were higher (2.39Â€ and 2.36â•–ppm) than at T2; the same was true for indoor CO concentrations (2.87Â€and 2.86â•–ppm). Personal exposure to CO was higher at T1 (3.42â•–ppm), followed by T0 and T2 (2.55 and 2.41â•–ppm, respectively). In all the sites, CO concentrations were higher inside homes and schools than outside (from 1.21 to 1.64 times). Higher concentrations were recorded inside public and private motor vehicles and kitchens. However, most measurements were lower than the 11â•–ppm 8-hour Mexican standard.

7.4.8â•…Respiratory and Olfactory Condition The frequency of respiratory diseases was high; during the campaign parents reported that 55% of their children had respiratory diseases at T2, with 20% at T1 and T0. Spirometry results showed that median flow (FEF25-75) was smaller at T1 and T0. Children’s observed health conditions were probably impacted by the local levels of air pollutants, as noticeable by the different reported levels at suburban and urban sites. Olfactory threshold results indicate that children from T0 have the poorest olfactory sensitivity. Children from the semirural site, T2, presented the lowest thresholds. These thresholds represented a 2.8-fold difference for T0 and a 1.6-fold difference for

216

Air Pollution Detection threshold

0 2 4 6 8 10 12 14

First quality threshold

**

Dilution

**

Dilution

0 2 4 6 8 10 12 14

T2

TT

T1

T0

T2

TT

T1

T0

Figure 7.9 Children olfactory threshold by site.

T1 (Figure 7.9). The differences in olfactory thresholds might also indicate that the adverse effects of air pollution on the olfactory system appear early in life.

7.4.9 Oxidative Stress in Children MPO enzyme plasma activity was significantly elevated in children living in T1 in comparison with those in T2 (57.8 versus 47.7 U/mg protein), and the related lipids damage expressed as lipoperoxidation products (TBARS) concentration was higher at T2 than at T0 and T1 (13.00, 9.01, and 9.44 µM, respectively). PON1 enzyme activity was higher at T2 than at T1 and T0 (0.122, 0.103, 0.099 nmol p-nitrofenol/mg protein, respectively), and this correlates with the greater presence of carbonylation in T2 children than at the other sites. Finally, the T1 site children showed low antioxidant status expressed by the lowest NTE reduction (Figure 7.10). A multivariate analysis showed significant associations among carbonylation and ozone and nitrogen oxide exposures as an expression of pollutant-related protein damage. NBT reduction was related to benzene exposure and having a mother who smokes, expressing a reduction of the antioxidant state associated with these exposures. TBARS production was associated with PM10 exposure and a mother who smokes. PON1 activity was associated with ozone and parents who smoke, and MPO activity was associated with methylcyclopentane and trichloroethylene exposures (Table 7.1). This study result raises the possibility that oxidative damage to lipids, proteins, and other biological effects in children may be related to local air pollution levels. These levels could be influenced by the MCMA pollutant PM plume, which is transported to long distances and thus affects a wide area of neighboring states (including T2 site children).

7.4.10 Oxidative Stress in Adults The results for adults indicate that CRP did not differ significantly among adults living in the three sites (2.05, 1.33, and 1.38 for T0, T1, and T2, respectively). CRP

217

Air Pollutants Exposure and Health Effects

Thiobarbituric acid reactive substances

Activity of myeloperoxidase (MPO) 80 60 40 20

20 15 10 5

0

T2

T1

T0

0

1

T2

5

p < 0.01

2

T1

10

p < 0.05 p < 0.0001

3

T0

nmol dinitrophenylhydrazones/mg

nmol formazan/mg

p < 0.0001

T2

T0

T1

T0

T2

Determination of carbonyl groups

Reduction of nitroblue tetrazolium p < 0.0001

T1

0

0

15

p < 0.05 p < 0.01

25

p < 0.05 μM TBARS

U MPO/mg

100

0.20 0.15 0.10 0.05

T2

T1

0.00

T0

nmol p-nitrophenol/mg

Activity of paraoxonase (PON1)

Figure 7.10 Oxidative stress markers in children by site.

is a sensitive, although nonspecific, marker for inflammation; high CRP levels constitute a risk factor for cardiovascular events in apparently healthy individuals (Tracy et al., 1997). In this case, CRP was not sensitive enough to express a differential inflammatory condition related to air pollution exposure. It is well known that serum CP and Cu vary, responding to inflammation and infectious events. The CP mean levels were higher at T0 than at T1 and T2 (91.4, 62.94,

218

Air Pollution

Table 7.1 Children’s Oxidative Stress Biomarkers and Air Pollutants Regression Modelsa Marker

Related Covariate

R

R2 b

p

MPO

Methylcyclopentane Trichloroethylene Mother smoker PM10 Ozone Nitrous oxide Ozone Mother smoker Father smoker Benzene Mother smoker

0.26

0.07

0.02

0.36

0.13

0.02

0.57

0.32

≤0.00

0.30

0.09

0.01

0.47

0.22

≤0.00

TBARS Carbonylation PON1

NBT

a b

Linear regression. R2 corrected.

and 57.24, respectively). This indicator may suggest either a greater inflammation response from the T0 population and/or higher Cu levels in comparison with the other studied sites (Mendez et al., 2004). The activities of the antioxidant enzymes GPx (77.10, 47.11, and 50.97 U/g of hemoglobin at T0, T1, and T2, respectively) and SOD (1625, 1124, and 1510 U/g of hemoglobin at T0, T1, and T2, respectively) were highest at T0 (Figure 7.11). This may be an acute response to the higher production of air pollution-related hydrogen peroxide and superoxide anions. Thus, it may not be surprising that these individuals developed protective antioxidant defenses. Nitrite levels were highest at T2 (71.59). Increased nitrite levels at T2 might be attributed to the activation of inducible isoforms of NO synthesis in leukocytes (neutrophils, eosinophils, basophils, and mononuclear phagocytes) (Abou-Seif and Youssef, 2004), because NO synthetase is expressed at very high levels in macrophages activated by exposures to bacterial lipopolysaccharide (LPS) (Sheffler et al., 1995), irritant air pollutants, or the consumption of nitrite-rich food common in the Mexican diet. For adults, the multivariate analysis showed significant associations among GPx and benzene, ozone, NO2, SO2, and living near a factory. CRP was associated with NO2, SO2, and the presence of new furniture in homes. Nitrites were correlated with 1,3-butadiene, insecticides, and PM10 exposures, and CP was correlated with 1,3-butadiene, dodecane, styrene, and new furniture (Table 7.2).

7.4.11 Cytokines In the case of cytokines, mixed reactions to air pollutants were observed, since not only were proinflammatory cytokines increased but also suppressive cytokines

219

Air Pollutants Exposure and Health Effects (a) 1800 1600 1400 1200 1000 800 600 400 200 0

T0

T1

T2

Sites (b)

100 80 60 40 20 0

T0

T1

T2

Sites

Figure 7.11 Oxidative stress markers in adults by site. Superoxide dismutase u/g of hemoglobin. T0 = Iztapalapa Distrito Federal, T1 = Tecamac Mexico, T2 = Tizayuca Hidalgo ANOVA. T0 vs T1 p = 0.001, and T0 vs T2 p = 0.539. (b) Gluthatione Peroxidase u/g of hemoglobin T0 = Iztapalapa Distrito Federal, T1 = Tecamac Mexico, T2 = Tizayuca Hidalgo ANOVA. T0 vs T1, and T2. p = 0.001.

were produced in significant amounts (Vega et al., 2007). Children from T2 showed higher levels of IL-6, IL-4, IFN-g, GM-CSF, and IL-2 in their serum samples, while those from T0 showed the lowest levels of all cytokines (Figure 7.12). The parents’ cytokines were highest at T1, except for IL-10, IFN-g, and GM-CSF, which were highest at T0. Children’s cytokine regression models showed an association between IL-4 and PM2.5, and NO2 exposures; and IL-6 was correlated with PM2.5, SO2, and PM10

220

Air Pollution

Tabel 7.2 Adults’ Oxidative Stress Biomarkers and Air Pollutants Regression Modelsa Marker GPx

CRP

Nitrites

CP

a b

Related Covariate Benzene O3 NO2 SO2 Factory close NO2 SO2 New furniture 1,3-Butadiene Insecticides PM10 1,3-Butadiene Dodecane Styrene New furniture

R

R2 b

p

0.68

0.43

≤0.00

0.33

0.08

0.01

0.42

0.14

0.01

0.38

0.11

≤0.00


exposures and living near a factory (Table 7.3). For adults, an important association between IL-4 and trichloroethylene and smoking was observed. GM-CSF and IL-10 were associated with ozone and smoking, and IL-12 was associated with home traffic density and limonene (Table 7.4). It is possible that some of the observed changes on seric cytokines may be related to contaminants other than those evaluated in this study, such as PAHs. PAHs are known to modulate cytochrome expression and immune responses (Elizondo and Vega, 2007), which may produce immunosuppression (Duramad et al., 2007), or asthma and allergy (Chung, 2001).

7.5 Conclusions A wide range of potentially harmful airborne pollutants emitted or produced by atmospheric processes in megacities makes it necessary to assess the exposure profiles of high-risk population subgroups. This approach is also necessary to study different interactions between pollutants and their early effects on biomarkers and other health conditions. The results obtained during the MILAGRO Campaign reported in this chapter illustrate the high frequency of many subclinical expressions related to air pollution, even though a significant reduction of MCMA air pollution levels has been achieved in recent times. It is also important to keep in mind that children are the most sensitive individuals in a population (Chung, 2001). More

221

Air Pollutants Exposure and Health Effects (a)

IL-6

(b) pg/mL/IL-12

pg/mL/IL-6

4000 3000 2000 1000 0

T0

Place

(c)

T1

T2

IL-4

T1

Place

T2

IF-N-Y

pg/mL/IL-4

30 20 10

3000 2500 2000 1500 1000 500 0

T0

300

T0

Place

T1

IL-2

200 100 0

T2

T0

(f )

Place

T1

T2

IL-10 2000

pg/mL/IL-10

pg/mL/IL-4 pg/mL/IL-2

(e)

6000 5000 4000 3000 2000 1000 0

(d)

40

0

IL-12

T0

Place

pg/ml GM-CSF

(g)

T1

1500

1500 1000 500 0

T2

T0

Place

T1

T2

GM-CSF

1000 500 0

T0

Place

T1

T2

Figure 7.12 Children serum cytokine levels by site.

research should be focused on how children are affected by air pollution and other xenobiotics. The air pollution-related indicators presented here may lead to future development or worsening of chronic diseases if more stringent controls and preventive programs are not established in the MCMA.

222

Air Pollution

Table 7.3 Children’s Cytokines and Air Pollutants Regression Modelsa IL-4 IL-6

a b

PM2 5 NO2 PM2 5 Factory near SO2 PM10

R

R2â•›b

p

0.24

0.04

0.06

0.86

0.78

≤0.00


Table 7.4 Adults’ Cytokines and Air Pollutants Regression Modelsa Covariates IL-4

Trichloroethylene

R

R2â•›b

p

0.74

0.52

≤0.00

0.42

0.13

0.02

0.55

0.26

≤0.00

0.58

0.29

≤0.00

Smoker GM-CSF

Ozone Smoker

IL-10

Ozone Smoker

IL-12

Traffic density Limonene

a b


Acknowledgments This project was partially funded by the Comisión Ambiental Metropolitana-Mexico, the Department of Occupational and Environmental Medicine, Göteborg University, the Human Exposure Research and Epidemiology, UFZ-Leipzig, NIH/Fogarty International Center 5 D43TW00644, the Centro Nacional de Investigación y Capacitación Ambiental-INE, and the Fondazione Salvatore Maugeri. The authors acknowledge Luisa T. Molina, Lars Barregard, René Lugo, Henry Wöhrnschimmel, Alejandro Treviño, José Samudio, Beatriz Cárdenas, Rosa Maria Berbabé, Felipe Angeles, Francisco Mandujano, Meike Schilde, and Paolo Sacco for their support and commentaries, and Jephte Cruz, Martha A. Hernández, Amilcar Torres, Martha Hernández, Gonzalo González, and Yazmín Affif for their collaboration during the campaign.


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