Acessibilidade / Reportar erro

Association of air pollution and hematologic parameters in children and adolescents

Abstracts

OBJECTIVE: To assess the relationship between air pollution and hematologic parameters in a population-based sample of children and adolescents. METHODS: This cross-sectional study was conducted in 2009-2010 among school students randomly selected from different areas of Isfahan city, the second largest and most air-polluted city in Iran. The association of air pollutant levels with hemoglobin, platelets, red and white blood cells (RBC and WBC, respectively) was determined by multiple linear and logistic regression analyses, after adjustment for age, gender, anthropometric measures, meteorological factors, and dietary and physical activity habits. RESULTS: The study participants consisted of 134 students (48.5% boys) with a mean age of 13.10±2.21 years. While the mean Pollutant Standards Index (PSI) was at moderate level, the mean particulate matter < 10 µm (PM10) was more than twice the normal level. Multiple linear regression analysis showed that PSI and most air pollutants, notably PM10, had significant negative relationship with hemoglobin and RBC count, and positive significant relationship with WBC and platelet counts. The odds ratio of elevated WBC increased as the quartiles of PM10, ozone and PSI increased, however these associations reached significant level only in the highest quartile of PM10 and PSI. The corresponding figures for hemoglobin and RBC were in opposite direction. CONCLUSIONS: The association of air pollutants with hematologic parameters and a possible pro-inflammatory state is highlighted. The presence of these associations with PM10 in a moderate mean PSI level underscores the necessity to re-examine environmental health policies for the pediatric age group.

Air pollution; cell blood count; atherosclerosis; inflammation; children; prevention


OBJETIVO: Avaliar a relação entre poluição atmosférica e parâmetros hematológicos em uma amostra populacional de crianças e adolescentes. MÉTODOS: Este estudo transversal foi realizado em 2009-2010 com estudantes escolhidos aleatoriamente de diversas áreas de Isfahan, a segunda maior e mais poluída cidade iraniana. A associação entre os níveis de poluentes do ar e os de hemoglobina, plaquetas, glóbulos brancos (GB) e glóbulos vermelhos (GV) foi determinada pelas análises linear múltipla e de regressão logística ajustadas para idade, sexo, medidas antropométricas, fatores meteorológicos, e hábitos alimentares e de atividade física. RESULTADOS: Participaram do estudo 134 estudantes (48,5% meninos), com idade média de 13,10±2,21 anos. Com níveis moderados de Pollutant Standards Index (PSI), a média de material particulado (particulate matter) < 10 µm (PM10) foi mais do que o dobro do normal. A análise de regressão linear demonstrou que o PSI e a maioria dos poluentes atmosféricos, especialmente PM10, estiveram negativamente relacionados com a contagem de hemoglobina e GV e positivamente relacionados com a contagem de GB e plaquetas. O odds ratio de uma elevação nos GB aumentou conforme os quartis de PM10, ozônio e PSI aumentavam, embora essas associações fossem significativas somente no quartil superior de PM10 e PSI. Os valores correspondentes de hemoglobina e GV seguiram a direção oposta. CONCLUSÕES: Destaca-se a associação dos poluentes atmosféricos com parâmetros hematológicos e um possível estado pró-inflamatório. A presença dessas associações com PM10 em níveis regulares de PSI enfatiza a necessidade de se reavaliar as políticas ambientais de saúde na faixa etária pediátrica.

Poluição do ar; contagem de células sanguíneas; aterosclerose; inflamação; crianças; prevenção


ORIGINAL ARTICLE

Association of air pollution and hematologic parameters in children and adolescents

Parinaz PoursafaI;Roya KelishadiII;Amin AminiIII;Abasgholi AminiIV;Mohammad Mehdi AminV;Mohammadreza LahijanzadehVI;Mohammadreza ModaresiVII

IMSc. Environmental Protection Engineer, Environment Research Center, Isfahan University of Medical Sciences, Isfahan, Iran. Department of Environmental Protection, Islamic Azad University, Science and Research Branch, Tehran, Iran

IIMD. Professor, Pediatrics, Pediatrics Department, Child Health Promotion Research Center, Isfahan University of Medical Sciences, Isfahan, Iran

IIIMD. Islamic Azad University, Najafabad Branch, Isfahan, Iran

IVMD. Associate professor, Pediatrics, Pediatrics Department, School of Medicine, Isfahan University of Medical Sciences, Isfahan, Iran

VPhD. Associate professor, Environmental Health Engineering, Department of Environmental Health Engineering, Environment Research Center, Isfahan University of Medical Sciences, Isfahan, Iran

VIMSc. Environmental Protection Engineer, Isfahan Provincial Directorate of Environmental Protection, Environmental Protection Department, Isfahan, Iran

VIIMD. Assistant professor, Pediatrics, Pediatrics Department, Child Health Promotion Research Center, Isfahan University of Medical Sciences, Isfahan, Iran

Correspondence Correspondence: Roya Kelishadi Pediatrics Department, Child Health Promotion Research Center Hezar Jerib Ave. – Isfahan University of Medical Sciences Isfahan – Iran Tel.: +98 (311) 792.2246 Fax: +98 (311) 669.4737 E-mail: kroya@aap.net, kelishadi@med.mui.ac.ir

ABSTRACT

OBJECTIVE: To assess the relationship between air pollution and hematologic parameters in a population-based sample of children and adolescents.

METHODS: This cross-sectional study was conducted in 2009-2010 among school students randomly selected from different areas of Isfahan city, the second largest and most air-polluted city in Iran. The association of air pollutant levels with hemoglobin, platelets, red and white blood cells (RBC and WBC, respectively) was determined by multiple linear and logistic regression analyses, after adjustment for age, gender, anthropometric measures, meteorological factors, and dietary and physical activity habits.

RESULTS: The study participants consisted of 134 students (48.5% boys) with a mean age of 13.10±2.21 years. While the mean Pollutant Standards Index (PSI) was at moderate level, the mean particulate matter < 10 µm (PM10) was more than twice the normal level. Multiple linear regression analysis showed that PSI and most air pollutants, notably PM10, had significant negative relationship with hemoglobin and RBC count, and positive significant relationship with WBC and platelet counts. The odds ratio of elevated WBC increased as the quartiles of PM10, ozone and PSI increased, however these associations reached significant level only in the highest quartile of PM10 and PSI. The corresponding figures for hemoglobin and RBC were in opposite direction.

CONCLUSIONS: The association of air pollutants with hematologic parameters and a possible pro-inflammatory state is highlighted. The presence of these associations with PM10 in a moderate mean PSI level underscores the necessity to re-examine environmental health policies for the pediatric age group.

Keywords: Air pollution, cell blood count, atherosclerosis, inflammation, children, prevention.

Introduction

A considerable part of the global burden of disease is attributable to preventable environmental exposures. In most countries, cardiovascular diseases impose the highest burden of disease, and their association with environmental factors, notably air pollution, is well documented,1 although the underlying mechanisms remain to be determined. Consistent with some previous findings, a recent experimental study showed for the first time that respiratory exposure to particulate matter enhances the process of atherogenesis2; thus, it might be the link between air pollution and cardiovascular diseases. Moreover, it is suggested that a pro-inflammatory state contributes to cardiometabolic risk factors, and the association of air pollution with these risk factors is documented both in adults3 and adolescents.4

Furthermore, some studies have suggested an association between hematological parameters and the pro-inflammatory state related to cardiometabolic risk factors. A population-based study in Taiwan found that a higher number of white blood cells (WBC) and red blood cells (RBC) increased the odds ratio (OR) of clustering of cardiometabolic risk factors.5 Such association is also suggested between platelet and WBC counts and clustering of cardiometabolic risk factors.6 Likewise, the association of hematologic parameters, notably WBC, with cardiometabolic risk factors is documented in children and adolescents.7,8

The relationship of air pollution with hematological factors remains controversial. While some studies reported the association of short-term9 and long-term10 exposure to air pollution with WBC count, some other studies did not confirm such association.11,12 It is suggested that differences in the extent of the response to air pollutants are influenced by the variation in susceptibility among individuals. For example, those with old age or underlying cardiovascular risk factors may show stronger associations.10,13 Children are particularly at risk when exposed to air pollution, because they receive a higher dose of pollutants than adults, with more extreme consequences.14,15 However, limited experience exists about the association of air pollutants with hematologic factors in the pediatric age group. Studying the effects of environmental factors on children's health can serve for future studies exploring the pathophysiologic mechanisms of adverse health effects and may offer strategies for primary prevention of chronic diseases. This study aimed to assess the relationship of air pollution and hematologic factors in the pediatric age group.

Methods

Participants

This cross-sectional study was conducted from November 2009 to February 2010 on the target population of children and adolescents aged 10-18 years residing in Isfahan, Iran's second largest and most air-polluted city. Eligible individuals were those who lived in areas of the city which had air pollution measurement stations, who had lived in that area for at least 6 months, and whose homes and schools were in the same area. Students who had a history of active or passive smoking, chronic disease or long-term medication use, or a history of acute infectious diseases in the past 2 weeks were not included in the study.

The study was conducted on 134 students. The sample size was calculated based on the correlation (r = 0.24) between air pollutants and blood cell counts found in a previous study16 and considering the statistical significance of 5%. Students were selected by random sampling, taking into account the proportion of the different types of schools (public/private) to avoid socioeconomic bias. Schools were randomly selected in each city area having air monitoring stations. Then, students from the chosen schools were allocated code numbers and randomly selected using random number tables.

The study was approved by the Research and Ethics Committee of the Faculty of Medicine, Isfahan University of Medical Sciences. Before the start of the study, written consent was obtained from parents and oral assent from students.

Study area

Isfahan is an industrial city with nearly 2 million inhabitants, located in the center of Iranian plateau, with an average altitude of 1,500 m above sea level, and bounded by a northwest-southeast mountain range of 3,000 m. The average monthly temperature is 16 °C, with a maximum of 29 °C in July and a minimum of 3 °C in December, and mild winds from the west and the south. Moreover, the air of the city of Isfahan is predominantly affected by industrial emissions and motor traffic, which can lead to a build-up of elevated concentrations of air pollutants during stagnant conditions.17

Clinical study and laboratory methods

According to government rules, blood collection from students cannot be done in schools. Therefore, the selected students were invited to health care centers. A trained nurse completed a questionnaire on demographic data, and physical examination was performed by a trained general practitioner, under the supervision of a pediatrician. Subcutaneous fat of the biceps and triceps muscles was measured with a skinfold caliper (Mojtahedi, Iran), and percent body fat was determined by bioelectrical impedance using a body fat monitor (Omron HBF-300, Japan).

For the assessment of dietary habits, the Healthy Eating Index (HEI) was computed as described before.4 Physical activity level was assessed by the international Physical Activity Questionnaire for Children, previously validated in Iranian children.18

While one of the parents accompanied his or her child, blood samples were taken from the antecubital vein. A complete blood profile, including hemoglobin, RBC, WBC and platelet counts, was measured using an automated cell counter (SYSMEX K-1000, Japan).

Air pollution data

After following the necessary procedures, we used the daily registered data of Isfahan Provincial Directorate of Environmental Protection, obtained from five air pollution measurement stations in Isfahan city. On the day of blood sampling, the data of the last seven 24-hour levels of air pollutants and Pollutant Standards Index (PSI) of the monitoring station located in the area of residence of each participant were recorded and included in the statistical analysis.4 Daily values pertaining to the main air pollutants, i.e. sulfur dioxide (SO2), ozone (O3), particulate matter < 10 µm (PM10), nitrogen dioxide (NO2), and carbon monoxide (CO), as well as to the PSI, mean daily temperature, sunlight duration, humidity, and wind speed were recorded. Particles in the air are a mixture of solids and liquid droplets that vary in size and are often referred to as "particulate matter." Particles less than 10 µm in diameter (PM10) pose the greatest health concern because they can pass through the nose and throat and get deep into the lungs. The PSI converts air pollution concentrations to a simple number between zero and 500 and assigns a descriptive term such as "good" or "moderate" to that value. The reference values of air pollutants and PSI are presented in the footer of Table 1.

Statistical analysis

SPSS for Windows (version 16.0, SPSS Inc., Chicago, IL, USA) was used for data analysis. We used log-transformed concentrations of air pollution markers to achieve normal distribution. The associations between air pollutants and hematologic parameters were assessed by multiple linear regression, after adjustment for age, gender, body mass index, waist circumference, meteorological factors, HEI, and physical activity level. The concentrations of biomarkers and air pollutants were categorized into quartiles, and the upper quartile was considered as elevated value. We examined the association of the dichotomized concentrations of hematologic parameters (upper quartile, y = 1 vs. lower quartile, y = 0) across the quartiles of air pollutants by using logistic regression analysis after adjustment for the abovementioned confounders. The significance level was set at p < 0.05.

Results

The study participants consisted of 134 students (48.5% boys) with a mean age of 13.10±2.21 years. Mean and standard deviation values of the variables studied are presented in Table 1. The mean hemoglobin level was 13.1±1.0 g/dL (range: 11-16.2 g/dL) and the mean WBC count was 7,373±1,800/mm3. The mean PSI value was at moderate level, i.e. an inappropriate level for sensitive groups. Mean levels of O3, NO2 and SO2 were much higher than acceptable values, and the mean PM10 level was remarkably high, reaching more than twice the normal level (120.48 vs. 50 µg/m2).

Multiple linear regression analysis showed that, after adjustment for confounding factors, PSI, and most air pollutants, notably PM10, had significant negative relationship with hemoglobin and RBC count, and significant positive relationship with WBC and platelet counts (Table 2).

The OR of elevated WBC increased as the quartiles of PM10, O3 and PSI increased, although these associations reached a significant level only in the highest quartile of PM10 and PSI. The corresponding figures for hemoglobin and RBC were in opposite direction, i.e. the OR was lower in the highest quartiles of PM10, O3 and PSI for WBC and in the lowest quartiles for hemoglobin and RBC (Table 3).

Discussion

This study, which, to the best of our knowledge, is the first of its kind in the pediatric age group, documented significant associations between exposure to air pollution and hematologic parameters in a population-based sample of children and adolescents.

Our findings are in line with an experimental study that revealed a significant decrease in hematocrit and a significant increase in leukocyte number in mice placed in cages with polluted air.19 Another experimental study showed that exposure to PM10 causes a systemic inflammatory response including stimulation of the bone marrow and progression of atherosclerosis. Given the key role of monocytes in atherogenesis, by migration into subendothelial lesions and appearing as foam cells, this study suggested that exposure to PM10 accelerates the process of atherosclerosis in relation to the amount of particles phagocytosed by alveolar macrophages.20 Our findings in children are also consistent with the Third National Health and Nutrition Examination Survey in the United States, conducted among adults aged 20-89 years, which showed significant association between WBC count and estimated local PM10 levels during 1 year.21

However, our findings contrast with those from a study in Turkey that compared hematological parameters before and after a period of exposure to heavy pollution and showed increased hemoglobin and hematocrit levels.22 This difference might be because of the shorter exposure to air pollutants and the higher age group of this study compared to ours. Moreover, the findings of the study in Turkey might be because of the accumulative effect of chronic air pollution and an acute episode of heavy pollution. Such concomitant effect is documented for chronic exposure to air pollution and chemical agents; in a study among 42 non-smoker petrol filling workers, chronic exposure to solvents like benzene and to pollutants like CO was associated with a significant rise in hemoglobin and RBC levels and a significant decrease in WBC levels.23

Our results are consistent with the findings of a study on the effects of indoor pollution on 8 to 13 year-old Indian children, which showed that living in households that cook with traditional biomass fuels was associated with low hemoglobin and RBC counts and raised WBC count.24 Health hazards of both indoor and outdoor air pollution depend on the pollutant type, its concentration in the air, length of exposure, other pollutants in the air, and individual susceptibility. Children are one the most vulnerable groups for such health impacts.

The findings of this study highlight the importance of adverse health effects of air pollution on children's health. The present study might provide confirmatory evidence of the pro-inflammatory state induced by air pollutants,25 and suggests that the association between air pollution and chronic diseases may be mediated through systemic inflammatory responses.

Our finding on the inverse association of air pollutants with hemoglobin level is in line with a study among an adult urban population in Canada.26 Contrary to these findings, a study in Denmark on 50 university students, aged 20-33 years, found positive associations between personal exposure to particulate matter < 2.5 µm (PM2.5) and both RBC and hemoglobin concentrations only in female students.27 The difference between our findings and those of this study might be because we could not measure ultrafine particles, however, as a study in Guatemala found, exposure to indoor air pollution resulting from the burning of biomass fuels was associated with elevation of hemoglobin concentration.28 Although we had no case of anemia and the statistical analyses were controlled for gender, we suggest that in future surveys the hematologic status of study participants and possible gender differences in the association of air pollutants with blood parameters should be addressed in more detail. We should also acknowledge that our study participants were much younger than those of the aforementioned studies, i.e. before the development of gender differences in the prevalence of anemia.

We found positive association of air pollutants and platelet counts, although we did not assess platelet activity and aggregation. However, the increase in platelets in relation to air pollutants may be a surrogate marker of early hematologic and hemostatic changes due to air pollutants. Experimental and human studies have proposed that the systemic pro-inflammatory and pro-coagulant response to inhalation of fine and ultrafine particulate matter suggests a role for platelet activation in such changes. However, some studies are inconsistent about the role of inflammation in this process. A human study found that air pollution increased platelet aggregation and coagulation activity but without clear effect on systemic inflammation. The study suggested that the prothrombotic effects may partly explain the effects of air pollution on ischemic cardiovascular diseases.29

A cross-over study among 29 participants with or without biking exercise and exposed to air pollutants did not find any significant association of air pollutants with hemoglobin, RBC and platelet count and markers of inflammation in healthy young adults.30 The associations of air pollutants with hematologic parameters in our study are consistent with the chronic effects of air pollutants on hematological factors in adults,16 hence our findings can be due to chronic exposure of children studied to air pollutants or due to the higher susceptibility of children to the health hazards of air pollutants.

In addition to suggested effects of air pollution on respiratory and immunologic diseases, and also on the early stages of atherosclerosis,4,31 the findings of our study propose an association of air pollutants with bone marrow activity. By considering the carcinogenic effects of air pollutants in children,32 our findings might be alarming for more worrisome effects of air pollution on children's health.

The findings of the present study may have implications for understanding the systemic effects and possible pro-inflammatory state induced by air pollutants; further studies in this regard are warranted.

Isfahan is the second most polluted industrial city in Iran, where the number of factories, cars and motorcycles is increasing.17 Although the urban air generally had a moderate level of PSI during the time period of this study, air pollutants had significant association with hematologic parameters. This association might be due to the susceptibility of children to environmental threats, and/or due to the noticeably high level of PM10 and other air pollutants as O3, NO2, and SO2. Moreover, this association might be due to the long-term exposure of the children studied to improper air quality year-round. Our findings are confirmatory evidence on the role of pediatricians to address environmental pediatrics health care needs and to improve the health status of children and adolescents.33

Study limitations and strengths

The main limitation of this study is that the findings from different analyses of air pollutants associated with hematologic factors should be interpreted with caution, given the cross-sectional nature of the associations. Such associations should be confirmed in future longitudinal studies. The existing equipment was unable to measure more specific particles such as PM2.5. Although we found significant association of larger particles (PM10) with the biomarkers studied, studying ultrafine particles might result in stronger associations. Another confounding variable which was not controlled was the possibility that there could be differences in the relative incidence of hemoglobinopathies among subsets of children living in the different regions where pollution indicators were measured, however the random sampling of the study reduces the possibility and effect of these confounding factors on the study findings. It should also be acknowledged that we did not study all hematologic parameters reflecting the bone marrow response. Furthermore, we measured systemic biomarkers, but more localized investigation, e.g. assessment of lung tissue in broncho-alveolar lavage, may yield better results.

The main strengths of this study are its novelty of enrolling of a very young age group and studying a population-based sample of healthy children, as well as assessing potential confounding factors and controlling them in statistical analysis for the study of the association between air pollutants and hematologic parameters.

Conclusion

Our findings highlight the association of hematologic parameters with PM

10 (which is larger than PM

2.5, usually considered more harmful) in a moderate mean PSI level (which is usually considered with few or no health effect for the general population) and a possible pro-inflammatory state. The presence of these associations with PM

10 in a moderate mean PSI level underscores the necessity to re-evaluate the environmental health policies and standards for the pediatric age group. The findings of this study should be confirmed in future longitudinal studies. Environmental protection concerns should be considered a top priority for primordial and primary prevention of chronic diseases.

References

1. Brook RD, Rajagopalan S, Pope CA 3rd, Brook JR, Bhatnagar A, Diez-Roux AV, et al. American Heart Association Council on Epidemiology and Prevention, Council on the Kidney in Cardiovascular Disease, and Council on Nutrition, Physical Activity and Metabolism. Particulate matter air pollution and cardiovascular disease: An update to the scientific statement from the American Heart Association. Circulation. 2010;121:2331-78.

2. Lund AK, Lucero J, Harman M, Madden MC, McDonald JD, Seagrave JC, et al. The Oxidized Low Density Lipoprotein Receptor Mediates Vascular Effects of Inhaled Vehicle Emissions. Am J Respir Crit Care Med. 2011 Apr 14. [Epub ahead of print]

3. Brook RD, Jerrett M, Brook JR, Bard RL, Finkelstein MM. The relationship between diabetes mellitus and traffic-related air pollution. J Occup Environ Med. 2008;50:32-8.

4. Kelishadi R, Mirghaffari N, Poursafa P, Gidding SS. Lifestyle and environmental factors associated with inflammation, oxidative stress and insulin resistance in children. Atherosclerosis. 2009;203:311-9.

5. Wang YY, Lin SY, Liu PH, Cheung BM, Lai WA. Association between hematological parameters and metabolic syndrome components in a Chinese population. J Diabetes Complications. 2004;18:322-7.

6. Jesri A, Okonofua EC, Egan BM. Platelet and white blood cell counts are elevated in patients with the metabolic syndrome. J Clin Hypertens (Greenwich). 2005;7:705-11.

7. Wu CZ, Hsiao FC, Lin JD, Su CC, Wang KS, Chu YM, et al. Relationship between white blood cell count and components of metabolic syndrome among young adolescents. Acta Diabetol. 2010;47:65-71.

8. Kelishadi R, Hashemipour M, Ashtijou P, Mirmoghtadaee P, Poursafa P, Khavarian N, et al. Association of cell blood counts and cardiometabolic risk factors among young obese children. Saudi Med J. 2010;3:406-12.

9. Riediker M. Cardiovascular effects of fine particulate matter components in highway patrol officers. Inhal Toxicol. 2007;19 (suppl):99-105.

10. Chen JC, Schwartz J. Metabolic syndrome and inflammatory responses to long-term particulate air pollutants. Environ Health Perspect. 2008;116:612-7.

11. Steinvil A, Kordova-Biezuner L, Shapira I, Berliner S, Rogowski O. Short-term exposure to air pollution and inflammation-sensitive biomarkers. Environ Res. 2008; 106:51-61.

12. Forbes LJ, Patel MD, Rudnicka AR, Cook DG, Bush T, Stedman JR, et al. Chronic exposure to outdoor air pollution and markers of systemic inflammation. Epidemiology. 2009;20:245-53.

13. Dubowsky SD, Suh H, Schwartz J, Coull BA, Gold DR. Diabetes, obesity, and hypertension may enhance associations between air pollution and markers of systemic inflammation. Environ Health Perspect. 2006;114:992-8.

14. Kim JJ. American Academy of pediatrics, committee on Environmental health. Ambient air pollution: health hazards to children. Pediatrics. 2004;114:1699-707.

15. Kelishadi R, Poursafa P. Air pollution and non-respiratory health hazards for children. Arch Med Sci. 2010;6:483-95.

16. Saadat M, Bahaoddini A. Hematological changes due to chronic exposure to natural gas leakage in polluted areas of Masjid-i-Sulaiman (Khozestan province, Iran). Ecotoxicol Environ Saf. 2004;58:273-6.

17. Talebi S M, Tavakoli T ,Ghinani A. Levels of PM10 and its chemical composition in the atmosphere of the city of Isfahan. Iran J Chem Engin. 2008;3:62-7.

18. Faghihimani Z, Nourian M, Nikkar AH, Farajzadegan Z, Khavariyan N, Ghatrehsamani S , et al. Validation of the Child and Adolescent International physical activity questionnaires in Iranian children and adolescents. ARYA Atherosclerosis. 2010; 5:163-6.

19. Gorriz A, Llacuna S, Riera M, Nadal J. Effects of air pollution on hematological and plasma parameters in Apodemus sylvaticus and Mus musculus. Arch Environ Contam Toxicol. 1996;31:153-8.

20. Goto Y, Hogg JC, Shih CH, Ishii H, Vincent R, van Eeden SF. Exposure to ambient particles accelerates monocyte release from bone marrow in atherosclerotic rabbits. Am J Physiol Lung Cell Mol Physiol. 2004;287:79-85.

21. Chen JC, Schwartz J. Metabolic syndrome and inflammatory responses to long-term particulate air pollutants. Environ Health Perspect. 2008; 116:612-7.

22. Baskurt OK, Levi E, Caglayan S, Dikmenoglu N, Kutman MN. Hematological and hemorheological effects of air pollution. Arch Environ Health. 1990;45:224-8.

23. Uzma N, Salar BM, Kumar BS, Aziz N, David MA, Reddy VD. Impact of organic solvents and environmental pollutants on the physiological function in petrol filling workers. Int J Environ Res Public Health. 2008;5:139-46.

24. Padhy PK, Padhi BK. Effects of biomass combustion smoke on hematological and antioxidant profile among children (8-13 years) in India. Inhal Toxicol. 2009;21:705-11.

25. Ruckerl R, Ibald-Mulli A, Koenig W. Air pollution and markers of inflammation and coagulation in patients with coronary heart disease. Am J Respir Crit Care Med. 2006; 173:432-41.

26. Goldberg MS, Bailar JC 3rd, Burnett RT, Brook JR, Tamblyn R, Bonvalot Y, et al. Identifying subgroups of the general population that may be susceptible to short-term increases in particulate air pollution: a time-series study in Montreal, Quebec. Res Rep Health Eff Inst. 2000; 97:115-20.

27. Sørensen M, Daneshvar B, Hansen M, Dragsted LO, Hertel O, Knudsen L, et al. Personal PM2.5 exposure and markers of oxidative stress in blood. Environ Health Perspect. 2003;111:161-6.

28. Neufeld LM, Haas JD, Ruel MT, Grajeda R, Naeher LP. Smoky indoor cooking fires are associated with elevated hemoglobin concentration in iron-deficient women. Rev Panam Salud Publica 2004; 15:110-8.

29. Rudez G, Janssen NA, Kilinc E, Leebeek FW, Gerlofs-Nijland ME, Spronk HM, et al. Effects of ambient air pollution on hemostasis and inflammation. Environ Health Perspect. 2009;117:995-1001.

30. Bräuner EV, Møller P, Barregard L, Dragsted LO, Glasius M, Wåhlin P, et al. Exposure to ambient concentrations of particulate air pollution does not influence vascular function or inflammatory pathways in young healthy individuals. Part Fibre Toxicol. 2008; 5:13.

31. Poursafa P, Kelishadi R, Lahijanzadeh A, Modaresi M, Javanmard SH, Assari R, et al. The relationship of air pollution and surrogate markers of endothelial dysfunction in a population-based sample of children. BMC Public Health. 2011;11:115.

32. Lin ZQ, Xi ZG, Yang DF, Chao FH, Zhang HS, Zhang W, et al. Oxidative damage to lung tissue and peripheral blood in endotracheal PM2.5-treated rats. Biomed Environ Sci. 2009;22:223-8.

33. Valenzuela PM, Matus MS, Araya GI, Paris E. Environmental pediatrics: an emerging issue. J Pediatr (Rio J). 2011; 87:89-99.

Manuscript submitted Mar 04 2011, accepted for publication Jun 02 2011.

No conflicts of interest declared concerning the publication of this article.

Suggested citation: Poursafa P, Kelishadi R, Amini A, Amini A, Amin MM, Lahijanzadeh M, et al. Association of air pollution and hematologic parameters in children and adolescents. J Pediatr (Rio J). 2011;87(4):350-6.

  • 1. Brook RD, Rajagopalan S, Pope CA 3rd, Brook JR, Bhatnagar A, Diez-Roux AV, et al. American Heart Association Council on Epidemiology and Prevention, Council on the Kidney in Cardiovascular Disease, and Council on Nutrition, Physical Activity and Metabolism. Particulate matter air pollution and cardiovascular disease: An update to the scientific statement from the American Heart Association. Circulation. 2010;121:2331-78.
  • 2. Lund AK, Lucero J, Harman M, Madden MC, McDonald JD, Seagrave JC, et al. The Oxidized Low Density Lipoprotein Receptor Mediates Vascular Effects of Inhaled Vehicle Emissions. Am J Respir Crit Care Med. 2011 Apr 14. [Epub ahead of print]
  • 3. Brook RD, Jerrett M, Brook JR, Bard RL, Finkelstein MM. The relationship between diabetes mellitus and traffic-related air pollution. J Occup Environ Med. 2008;50:32-8.
  • 4. Kelishadi R, Mirghaffari N, Poursafa P, Gidding SS. Lifestyle and environmental factors associated with inflammation, oxidative stress and insulin resistance in children. Atherosclerosis. 2009;203:311-9.
  • 5. Wang YY, Lin SY, Liu PH, Cheung BM, Lai WA. Association between hematological parameters and metabolic syndrome components in a Chinese population. J Diabetes Complications. 2004;18:322-7.
  • 6. Jesri A, Okonofua EC, Egan BM. Platelet and white blood cell counts are elevated in patients with the metabolic syndrome. J Clin Hypertens (Greenwich). 2005;7:705-11.
  • 7. Wu CZ, Hsiao FC, Lin JD, Su CC, Wang KS, Chu YM, et al. Relationship between white blood cell count and components of metabolic syndrome among young adolescents. Acta Diabetol. 2010;47:65-71.
  • 8. Kelishadi R, Hashemipour M, Ashtijou P, Mirmoghtadaee P, Poursafa P, Khavarian N, et al. Association of cell blood counts and cardiometabolic risk factors among young obese children. Saudi Med J. 2010;3:406-12.
  • 9. Riediker M. Cardiovascular effects of fine particulate matter components in highway patrol officers. Inhal Toxicol. 2007;19 (suppl):99-105.
  • 10. Chen JC, Schwartz J. Metabolic syndrome and inflammatory responses to long-term particulate air pollutants. Environ Health Perspect. 2008;116:612-7.
  • 11. Steinvil A, Kordova-Biezuner L, Shapira I, Berliner S, Rogowski O. Short-term exposure to air pollution and inflammation-sensitive biomarkers. Environ Res. 2008; 106:51-61.
  • 12. Forbes LJ, Patel MD, Rudnicka AR, Cook DG, Bush T, Stedman JR, et al. Chronic exposure to outdoor air pollution and markers of systemic inflammation. Epidemiology. 2009;20:245-53.
  • 13. Dubowsky SD, Suh H, Schwartz J, Coull BA, Gold DR. Diabetes, obesity, and hypertension may enhance associations between air pollution and markers of systemic inflammation. Environ Health Perspect. 2006;114:992-8.
  • 14. Kim JJ. American Academy of pediatrics, committee on Environmental health. Ambient air pollution: health hazards to children. Pediatrics. 2004;114:1699-707.
  • 15. Kelishadi R, Poursafa P. Air pollution and non-respiratory health hazards for children. Arch Med Sci. 2010;6:483-95.
  • 16. Saadat M, Bahaoddini A. Hematological changes due to chronic exposure to natural gas leakage in polluted areas of Masjid-i-Sulaiman (Khozestan province, Iran). Ecotoxicol Environ Saf. 2004;58:273-6.
  • 17. Talebi S M, Tavakoli T ,Ghinani A. Levels of PM10 and its chemical composition in the atmosphere of the city of Isfahan. Iran J Chem Engin. 2008;3:62-7.
  • 18. Faghihimani Z, Nourian M, Nikkar AH, Farajzadegan Z, Khavariyan N, Ghatrehsamani S , et al. Validation of the Child and Adolescent International physical activity questionnaires in Iranian children and adolescents. ARYA Atherosclerosis. 2010; 5:163-6.
  • 19. Gorriz A, Llacuna S, Riera M, Nadal J. Effects of air pollution on hematological and plasma parameters in Apodemus sylvaticus and Mus musculus. Arch Environ Contam Toxicol. 1996;31:153-8.
  • 20. Goto Y, Hogg JC, Shih CH, Ishii H, Vincent R, van Eeden SF. Exposure to ambient particles accelerates monocyte release from bone marrow in atherosclerotic rabbits. Am J Physiol Lung Cell Mol Physiol. 2004;287:79-85.
  • 21. Chen JC, Schwartz J. Metabolic syndrome and inflammatory responses to long-term particulate air pollutants. Environ Health Perspect. 2008; 116:612-7.
  • 22. Baskurt OK, Levi E, Caglayan S, Dikmenoglu N, Kutman MN. Hematological and hemorheological effects of air pollution. Arch Environ Health. 1990;45:224-8.
  • 23. Uzma N, Salar BM, Kumar BS, Aziz N, David MA, Reddy VD. Impact of organic solvents and environmental pollutants on the physiological function in petrol filling workers. Int J Environ Res Public Health. 2008;5:139-46.
  • 24. Padhy PK, Padhi BK. Effects of biomass combustion smoke on hematological and antioxidant profile among children (8-13 years) in India. Inhal Toxicol. 2009;21:705-11.
  • 25. Ruckerl R, Ibald-Mulli A, Koenig W. Air pollution and markers of inflammation and coagulation in patients with coronary heart disease. Am J Respir Crit Care Med. 2006; 173:432-41.
  • 26. Goldberg MS, Bailar JC 3rd, Burnett RT, Brook JR, Tamblyn R, Bonvalot Y, et al. Identifying subgroups of the general population that may be susceptible to short-term increases in particulate air pollution: a time-series study in Montreal, Quebec. Res Rep Health Eff Inst. 2000; 97:115-20.
  • 27. Sřrensen M, Daneshvar B, Hansen M, Dragsted LO, Hertel O, Knudsen L, et al. Personal PM2.5 exposure and markers of oxidative stress in blood. Environ Health Perspect. 2003;111:161-6.
  • 28. Neufeld LM, Haas JD, Ruel MT, Grajeda R, Naeher LP. Smoky indoor cooking fires are associated with elevated hemoglobin concentration in iron-deficient women. Rev Panam Salud Publica 2004; 15:110-8.
  • 29. Rudez G, Janssen NA, Kilinc E, Leebeek FW, Gerlofs-Nijland ME, Spronk HM, et al. Effects of ambient air pollution on hemostasis and inflammation. Environ Health Perspect. 2009;117:995-1001.
  • 30. Bräuner EV, Mřller P, Barregard L, Dragsted LO, Glasius M, Wĺhlin P, et al. Exposure to ambient concentrations of particulate air pollution does not influence vascular function or inflammatory pathways in young healthy individuals. Part Fibre Toxicol. 2008; 5:13.
  • 31. Poursafa P, Kelishadi R, Lahijanzadeh A, Modaresi M, Javanmard SH, Assari R, et al. The relationship of air pollution and surrogate markers of endothelial dysfunction in a population-based sample of children. BMC Public Health. 2011;11:115.
  • 32. Lin ZQ, Xi ZG, Yang DF, Chao FH, Zhang HS, Zhang W, et al. Oxidative damage to lung tissue and peripheral blood in endotracheal PM2.5-treated rats. Biomed Environ Sci. 2009;22:223-8.
  • 33. Valenzuela PM, Matus MS, Araya GI, Paris E. Environmental pediatrics: an emerging issue. J Pediatr (Rio J). 2011; 87:89-99.
  • Correspondence:

    Roya Kelishadi
    Pediatrics Department, Child Health Promotion Research Center
    Hezar Jerib Ave. – Isfahan University of Medical Sciences
    Isfahan – Iran
    Tel.: +98 (311) 792.2246
    Fax: +98 (311) 669.4737
    E-mail:
  • Publication Dates

    • Publication in this collection
      12 Sept 2011
    • Date of issue
      Aug 2011

    History

    • Accepted
      02 June 2011
    • Received
      04 Mar 2011
    Sociedade Brasileira de Pediatria Av. Carlos Gomes, 328 cj. 304, 90480-000 Porto Alegre RS Brazil, Tel.: +55 51 3328-9520 - Porto Alegre - RS - Brazil
    E-mail: jped@jped.com.br