The Health Effects Of Exposure

Published Date: 02 Nov 2017

INTRODUCTION

The health effects of exposure to air pollutants have been extensively documented and reviewed (Brunekreef & Holgate, 2002; Lacasaña, et al., 2005). The health impact of air pollutant is much higher for children than for adults, as their metabolic rate is higher than adults, which means that they breathe in more air per unit of body weight and are generally more susceptible to the effects of air pollutant (Faustman, et al., 2000; Mendell & Heath, 2005; World Health Organization, 2006). Therefore, their exposure is a major health concern.

In the developed countries, the average length of school year ranges from 167 – 208 days (Sargent, et al., 2013), and the duration of school day for primary school ranges between 4.5 – 8 hours (Sargent, et al., 2013). For those in Hong Kong, there are no less than 190 schools days for whole-day schools (Education Bureau, 2005), and the school hours is around 7 hours per day. The data above indicates that children spend a measurable fraction of their time at school, and spending a considerable fraction of their school day breathing indoor air. Poor indoor air quality can leads to an increased incidence of health related symptoms, which in turn can lead to an increase in absenteeism and a loss of concentration (Mendell & Heath, 2005; Shendell, et al., 2004; Croome, et al., 2008).

There are many factors which affect indoor air quality, such as emissions from indoor sources, the operation of ventilation systems and the penetration of outdoor air pollutants indoors (Wallace, 1996; Vette, et al., 2001; Guo, et al., 2008). In the absence of major indoor source, indoor air quality is directly linked to the outdoor air quality.

Previous studies indicated that exposure to traffic is one of the principal contributors to air pollution in urban areas and have a significant effect on indoor environment (Wjst, et al., 1993) (van Wijnen & van der Zee, 1998; Fischer, et al., 2000; Martuzevicius, et al., 2008). Vehicular pollutants from outdoor environment can migrate to the indoor environment through ventilation intakes, open doors and windows, and leaks in the building envelope.

Studies have sought an association between vehicular pollutants and non-allergic respiratory morbidity. Janssen, et al., 2003 reported on 24 schools located within 400 m of busy motorways in the Netherlands; the study included 2503 schoolchildren aged 7–12 years. PM2.5, soot and nitrogen dioxide were measured in the schools for a year. Non-allergic respiratory symptoms (such as current phlegm and current bronchitis) were increased near motorways with high traffic counts of lorries, not cars. The adverse effects on health were mostly restricted to allergic, sensitized or bronchial-hyperreactive children. A study of 843 children from 8 Austrian communities measured nitrogen dioxide as a traffic indicator (Studnicka, et al., 1997). Increased prevalence of cough (apart from cold), was associated with high levels of nitrogen dioxide. Studies have investigated the association between transport-related air pollution and mortality. Katsouyanni, et al., 2001 reported the combined estimate for an increase in the daily number of deaths associated with a 10-µg/m3 increase in daily black smoke concentrations as 0.6%. A review by (Jones, 1999) showed that  indoor air is affected by both indoor and outdoor sources, and that traffic accounts for more than half the amount of combustion-related pollutants originating outdoors in urban environments.

With a land mass of 1,104km2 and a population of more than 7.1millon (Census and Statistics Department, 2012), Hong Kong is one of the most densely populated cities in the world. There were 630,281 vehicles licensed at the end of 2011, The average kilometrage per day per licensed vehicle was 54.66 km (Transport Department, 2011). High vehicle density in the crowded city can lead to adverse pollution problems (Ning, et al., 2012). Diesel vehicles are treated as the major source of different air pollutants (e.g. nitrogen oxide & black carbon) and fine particles (Kagawa, 2002; Kerminen, et al., 1997). Roadways with heavy traffic are close to sidewalks, residential and commercial buidlings and schools. Traffic emissions are trapped within street canyons formed by high-rise buildings, leading to poor dispersion and high, frequent human exposure. 

In summary, there is substantial exposure to traffic-related air pollution that can result in serious health impacts, children are at greater risk of experiencing health problems from this exposure. The air quality in schools has important health implication and a healthy indoor environments of school are required to reduce health risks and for better student performance.

OBJECTIVE

LITERATURE REVIEW

Outdoor Air Pollutants – health impacts and their source

Particulate Matters

Previous studies consistently indicated that outdoor particulate matter (PM) was the most important source of PM measured indoors (Jamriska, et al., 2000) (Koponen, et al., 2001) (Sawant, et al., 2004) (Martuzevicius, et al., 2008). Outdoor airborne particulates can readily penetrate indoor environments through cracks, opening windows and doors (Chao, et al., 1998). Therefore, outdoor

Several epidemiological studies have reported the adverse health effects of indoor PM concentrations. Exposure to high PM concentrations has been associated with increase in mortality and a number of pulmonary effects (Schwartz, et al., 1996) (Pope, et al., 2002) (World Health Organization, 2003) (M.R. Ashmore & C. Dimitroulopoulou, 2009)

Ultrafine Particle

Ultrafine particles (UFPs) are defined as particle with less than 100 nm in aerodynamic diameter. Despite their minimal contribution to the regulatory mass – based PM measure (PM2.5 or PM10), UFPs dominate the particle number size distribution. Given their tiny size, UFPs can penetrate via lungs, to the respiratory system and even transfer to extrapulmonary organs, including the central nervous system (Oberdörster, et al., 2004; Elder & Oberdörster, 2006; Elder, et al., 2006). Other studies indicate that UFP exposure shows a strong association with adverse effects on respiratory and cardiovascular health. (Peters, et al., 1997; Gilmour, et al., 2004; McCreanor, et al., 2007; Araujo, et al., 2008).

Vehicular emission has been shown to be one of the origins of UFPs. A large portion of PM emitted from combustion of motor engine occurs in the PM1.0 (diameter < 1µm) size range, with mass median diameter between 100 – 200nm (Kleeman, et al., 2000; Robert, et al., 2007a; Robert, et al., 2007b) and number median diameter around 20 nm (Janhäll, et al., 2004; Kittelson, et al., 2004). At a near-road location, UFPs were observed to have a magnified response to roadway emissions compared with larger particle sizes (Molnar, et al., 2002). Other studies have observed a strong spatial gradient associated with UFPs, exponentially decreasing with distance from major roadways (Hitchins, et al., 2000; Zhu, et al., 2002a; Zhu, et al., 2002b; Beckerman, et al., 2007). These results suggest that traffic is a major source of UFPs and heavily influences air concentrations in the nearby vicinity of a major roadway.

Nitrogen Oxides

Nitrogen oxides (NOx) is a generic term for nitric oxide (NO) and nitrogen dioxide (NO2) (HKEPD, 2005a). Automobiles are the main source of NOx in urban environment (Colvile, et al., 2001).

1) N2 + O2 → NO2

2) 2NO + O2 → 2NO2

Apart from primary emissions of combustion process in motor engine, NO2 can also be formed by oxidation of the NO emitted by vehicles via a photochemical process involving volatile organic compounds (VOCs) emitted by vehicles or other sources, and/or ozone present in the ambient air (HKEPD, 2011b).

NO + O3 → NO2 + O2

NO + HO2 → NO2 + OH

NO + RO2 → NO2 + RO

NOx is one of the major precursors for the formation of ground-level ozone, nitrate particles and acid aerosols which trigger chronic respiratory diseases (Delfino, 2002). Exposure to NO2 has been associated with the increase in non-accidental mortality in several time-series studies (Peters & Pope, 2002; Brook, et al., 2007; Beelen, et al., 2008).

According the Environmental Protection Department (EPD), total NOx emission in Hong Kong was 114,000 tonnes in 2011, while vehicular emission of NOx accounted for 29% of the total emission (HKEPD, 2011a), while emission from electric utilities and navigation are other major source of NOx.

Table - 2011 Hong Kong NOx Emission Inventory

Pollutant Source Categories

(Unit: Tonnes)

(Unit: %)

Public Electricity Generation

30,000

26%

Road Transport

32,700

29%

Navigation

37,700

33%

Civil Aviation

4,770

4%

Other Fuel Combustion [1] 

9,290

8%

Total

114,000

100%

Source: HKEPD, 2011

Sulfur Dioxide

Sulfur Dioxide (SO2) is the predominant anthropogenic sulfur-containing air pollutant. Being a colourless, reactive gas, SO2 is odourless at low concentrations but has a pungent smell at very high concentrations.

SO2 is a respiratory irritant and bronchoconstrictor, and has been associated with cardiovascular abnormalities including decrease in heart rate variability (Tunnicliffe, et al., 2001). Strong short- term association of ambient SO2 with increased risk of cardiorespiratory mortality and morbidity have been shown in Europe (Katsouyanni, et al., 1997), North America (Burnett, et al., 2000). Acute health effects of SO2 has been examined in four Asian cities, including Hong Kong (Kan, et al., 2010).

Thanks to the introduction of Euro V diesel in 2007 (sulfur content is capped at 0.001% ), SO2 emission from vehicles has been substantially reduced (figure 1) (HKEPD, 2005b). As compared to 1999, the 2010 SO2 level at the roadside was reduced by 63%. The SO2 levels registered by roadside air monitoring stations are now broadly comparable to those by general air quality monitoring stations (figure 2) (HKEPD, 2011b). Road transport contributes little to SO2 emission compared to power plant and vessels, with 207 tonnes SO2 emitted (0.6% of total emission) in 2011 (HKEPD, 2011a).

Figure - Vehicular SO2 Emission from 1997 to 2011

Figure – Trends of the concentration levels of SO2 at General and Roadside Monitoring Stations

Ozone

Ozone (O3) is a colorless gas in the atmosphere, a stable molecule composed of three oxygen atoms. Ozone can be good or bad to human health depending on where they are in the atmosphere:

Stratospheric ozone forms a series layer of low-density air containing 300 – 500 ppb of ozone (ozone layer), shielding the Earth’s surface from the sun’s ultraviolet (UV) radiation (<0.28 µm). If the ozone layer were removed, overexposure to UV radiation would lead to skin cancer. Therefore, ozone in stratosphere acts as a beneficial UV shield, protecting us from the solar harmful UV radiation.

However, tropospheric ozone is regarded as a harmful air pollutant. According to United States Environmental Protection Agency (USEPA), ozone is a strong oxidant and "breathing ozone can trigger a variety of health problems including chest pain, coughing, throat irritation, and congestion. It can worsen bronchitis, emphysema, and asthma. Ground level ozone also can reduce lung function and inflame the linings of the lungs. Repeated exposure may permanently scar lung tissue (USEPA, 2012)."

"People with lung disease, children, older adults, and people who are active outdoors may be particularly sensitive to ozone. Children are at greatest risk from exposure to ozone because their lungs are still developing and they are more likely to be active outdoors when ozone levels are high, which increases their exposure (USEPA, 2012)."

Ground-level O3 is a secondary pollutant, and is formed as a result of the photolysis involving NOx and VOCs in the presence of sunlight.

NO2 + hv → NO + O

O + O2 + M → O3 + M

Reaction (7) is the significant source of O3 in the atmosphere. Once formed, O3 reacts with NO to regenerate NO2:

O3 + NO → NO2 + O2

If NO is oxidized by other oxidants originated from VOC (e.g. formaldehyde, ethane) in the atmosphere, O3 would accumulates.

HO2∙ + NO → NO2 + HO∙

RO2∙ + NO → NO2 + RO∙

Net of (6)+(7)+(9): HO2∙ + O2 → O3 + HO∙

Net of (6)+(7)+(10): RO2∙ + O2 → O3 + RO∙