Effects of Polluted Air - Part 2

Air pollution affects both morbidity and mortality. The level of pollutants varies with location, altitude, temperature and wind patterns. The effect of air pollution is equally variable, the more susceptible an individual, the greater the effects of pollution. Exposure to high density traffic – nearness to roads with high traffic volumes as well as high diesel exhaust levels – also contribute to the impact of air pollution. The ultrafine particles of PM which at 2.5 microns is about 3% of the diameter of a human hair, especially can be inhaled and get into the blood stream and thence to the organs and cause damage therein. PM in particular has been linked to heart disease, stroke, cancer and kidney disease and has been listed by the World Health Organization (WHO) as an environmental carcinogen.

The consequence of exposure to air pollution and its severity of effects begins with subclinical effects and then increases through

  • impaired pulmonary function

  • symptoms

  • medication requirement and use

  • reduced physical performance

  • physician office visits

  • emergency room visits

  • hospital admissions

  • mortality

Recent research has shown additional effects of air pollution. These include:

Pre-birth effects

Research has indicated that pollution also affects the unborn child. Maternal thyroid function during pregnancy affects both growth and cognition of the fetus. Now it has been shown that soot and dust affects thyroid development in fetuses, prior to birth. Data on over 2000 newborns, enrolled in the Children’s Health Study was anlayzed using blood tests taken immediately after birth and corelated with monthly exposure to air pollution indicators throughout the mothers’ pregnancy. The researchers checked blood levels of total thyroxine, a hormone secreted by the thyroid gland. When exposure to PM increased by 16mcg/m3, the thyroxine increased by 7.5% above average levels in babies. PM was the only pollutant associated with this change and it was noted that the fetuses’ thyroid gland were particularly susceptible from early to mid-pregnancy.1

The latest research of healthy, non-smoking pregnant women found that their placenta contained carbon particles.2 Exposure to PM 2.5 during the third trimester of pregnancy was associated with elevated blood pressure in the children from age 3 to 9 years. After adjusting for birth weight and maternal smoking, children exposed to high levels of PM 2.5 in the womb during the third trimester were 61% more likely to have elevated systolic blood pressure in childhood than those who were exposed to low levels,

Yet another study found that prenatal exposure to NOx resulted in reduced lung function in children, particularly boys.3

Exposure to environmental pollutants during pregnancy has been known to increase the risk of asthma in children.4-6

DNA damage

Telomeres tend to shorten with age and this is consistent with age-related DNA. However air pollution can also lead to shortening telomeres, a sign of DNA damage. One of the components of air pollution is polycyclic aromatic hydrocarbons (PAHs), from vehicles exhaust. Children and adolescents living in Fresno, California, were chosen since Fresno is the second most polluted city in the USA. The study involved measuring their telomere lengths. The researchers found an inverse relationship, that is the greater the exposure to PAHs, the more the telomeres decreased.7

Cardiovascular disease

Exposure to air pollution causes atherosclerosic resulting in cardiovascular diseases that include myocardial infarction, arrhythmias and heart failure.8 A study of 89 men and women was undertaken to analyse the association between ozone exposure and cadiopulmonary mechanisms. The year-long study looked for biomarkers indicating inflammation and oxidative stress, arterial stiffness, thrombotic factors and measured both spirometry and blood pressure over four sessions.9 It found that exposure to ozone increased platelet activation, raised blood pressure and influenced pulmonary function. It also found that these effects were seen at lower levels of ozone exposure that affected the respiratory system. A 10 ppb increase in 24-hour ozone was associated with

  • 2.8 % increase in diastolic blood pressure

  • 18.1 % in FeNO, a marker of pulmonary inflammation, and

  • 31 % in exhaled breath condensate nitrate and nitrite

Zhao and colleagues10 did a systematic review and meta-analysis to determine the relationship between short-term exposure to PM (10 and 2.5), nitrogen dioxide, carbon monoxide, ozone and sulfur dioxide and the onset of cardiac arrest. They found no association with carbon monoxide or sulfur dioxide. They did find that while NO2 and O3 were significantly associated with an increased risk, the greatest risk came from PM.

Respiratory deficits and disease

The process of impaired pulmonary function begins with irritation of the respiratory system that leads to

  • reduction in lung function

  • inflammation and damage to the lining of the lungs

  • increased susceptibility to infection; exacerbation of lung disease (asthma, COPD)

  • permanent lung damage

  • acceleration of the normal decline in lung function that occurs with age.

The process also involves

  • symptoms

  • medication requirement and use

  • reduced physical performance

  • physician office visits

  • emergency room visits

  • hospital admissions, and finally

  • mortality.

Children aged 10 years of age were studied over a period of eight years to determine whether air pollution affected lung function.11 After adjusting for potential confounders and modifiers the researchers found that lung function, determined by FEV1 and other spirometric measures were impacted by nitrogen dioxide, acid vapour, PM 2.5 and carbon. They determined that current levels of air pollution have adverse effects on lung development resulting in “clinically significant deficits in attained FEV1" as the children reached adulthood.

Rice and colleagues did a long-term study of lung function of children from birth to 7.7 years. They concluded that lung impairment increased progressively with proximity to a major roads and with duration of exposure. Both FEV1 and FVC were affected and the authors suggest that air pollution impacts lung growth and lung function.12 Traffic-related pollution increased the risk of asthma in children and proximity to high traffic roads increased the risk.13

Inhalation of ultrafine PM from diesel traffic resulted in nasal irritation, airway hyper-responsiveness, airway inflammation, oxidative stress and it further magnified the allergic responses. Studies on the effects of long-term exposure to PM and asthma prevalence and morbidity in children concluded that children who were exposed to higher PM levels had an increased prevalence of asthma and its associated morbidity.14-16

. . . to be continued

Abbreviations

CO carbon monoxide, COPD chronic obstructive pulmonary disease, FeNO fraction of exhaled nitric oxide, FEV1 forced expiratory volume in one second, FVC forced vital capacity. mcg/m3 micrograms per cubic meter, NOx nitric oxides, O3 ozone, ppb parts per billion, PM particulate matter 2.5 mcg, PAH polycyclic aromatic hydrocarbons

References

  1. Howe CG, Eckel SP et al. Association of prenatal exposure to ambient and traffic-related air pollution with newborn thyroid function: Findings From the Children’s Health Study. JAMA Network Open, 2018 DOI: 10.1001/jamanetworkopen.2018.2172

  2. Zhang M, Mueller NT et al. Maternal exposure to ambient particulate matter ≤2.5 µm during pregnancy and the risk for high blood pressure in childhood. Hypertension, 2018; HYPERTENSIONAHA.117.10944 DOI: 10.1161/HYPERTENSIONAHA.117.10944

  3. Bose S, Rosa MJ et al. Prenatal nitrate air pollution exposure and reduced child lung function: Timing and fetal sex effects. Environ Res. 2018;167:591-597. doi: 10.1016/j.envres.2018.08.019

  4. Lavigne É, Bélair MA, et al. Effect modification of perinatal exposure to air pollution and childhood asthma incidence. Eur Respir J. 2018 Feb 1. pii: 1701884. doi: 10.1183/13993003.01884-2017.

  5. Hehua Z, Qing C, et al. The impact of prenatal exposure to air pollution on childhood wheezing and asthma: A systematic review. Environ Res. 2017 Nov;159:519-530. doi: 10.1016/j.envres.2017.08.038

  6. Lee A, Leon Hsu HH, et al. Prenatal fine particulate exposure and early childhood asthma: Effect of maternal stress and fetal sex. J Allergy Clin Immunol. 2018 May;141(5):1880-1886. doi: 10.1016/j.jaci.2017.07.017

  7. Lee EY, Lin J et al. Traffic-related air pollution and telomere length in children and adolescents living in Fresno, CA: A pilot study. J Occup Environ Med, 2017; 59 (5): 446 DOI: 10.1097/JOM.0000000000000996

  8. Münzel T, Gori T, et al. Effects of gaseous and solid constituents of air pollution on endothelial function. European Heart Journal, 2018; DOI: 10.1093/eurheartj/ehy481

  9. Day DB, Xiang J et al. Association of ozone exposure with cardiorespiratory pathophysiologic mechanisms in healthy adults. JAMA Internal Medicine, 2017; DOI: 10.1001/jamainternmed.2017.2842

  10. Zhao R, Chen S et al. The impact of short-term exposure to air pollutants on the onset of out-of-hospital cardiac arrest: A systematic review and meta-analysis. Int J Cardiol. 2017 Jan 1;226:110-117. doi: 10.1016/j.ijcard.2016.10.053.

  11. Gauderman WJ, Avol E et al. The effect of air pollution on lung development from 10 to 18 years of age. N Engl J Med. 2004;351:1057-1067.

  12. Rice MB, Rifas-Shiman SL et al. Lifetime exposure to ambient pollution and lung function in children. Am J Respir Crit Care Med. 2016;193:881-888

  13. Rice MB, Rifas-Shiman SL et al. Lifetime air pollution exposure and asthma in a pediatric birth cohort. J Allergy Clinical Immunology, 2018; DOI: 10.1016/j.jaci.2017.11.062

  14. Keet CA, Keller JP and Peng RD. Long-term coarse particulate matter exposure Is associated with asthma among children in Medicaid. AJRCCM 2018; 197(6) https://doi.org/10.1164/rccm.201706-1267OC

  15. Sbihi H, Tamburic L et al. Perinatal air pollution exposure and development of asthma from birth to age 10 years. Eur Resp J. DOI: 10.1183/13993003.00746-2015

  16. Brandt EB, Kovacic MB, et al. Diesel exhaust particle induction of IL-17A contributes to severe asthma. J Allergy Clin Immunol. 2013;132(5):1194–2042.