Question 2 of 7: SO 2 Flue-Gas Concentration and Health/Ecological Impacts of Air Pollutants

Question 2: SO₂ Flue-Gas Concentration and Health/Ecological Impacts of Air Pollutants (20 marks)

Question text not reproduced: the examination questions are © Engineers and Geoscientists BC. Open the official past paper (linked at the top of this page) to read the question, then follow the worked solution below.

(i) SO₂ Concentration in the Flue Gas

Given. Combustion of a sulfur-bearing hydrocarbon fuel with stoichiometric oxygen:

Find. The SO₂ concentration in the resulting flue gas (ppmv and vol.%).

Approach. Back-calculate the moles of sulphur from the 3%-by-mass fuel specification, balance the stoichiometric combustion of both the hydrocarbon and the sulphur, build up the total flue-gas mole count (CO₂ + H₂O + SO₂ + N₂, no excess O₂), and take the SO₂ mole fraction.

1. Molar mass and mass of the hydrocarbon. $M_{HC} = 7(12.01)+13(1.008) = 97.17\ \text{g/mol}$, so $m_{HC} = 100(97.17) = 9717.4\ \text{g}$.
2. Back out the sulphur. Since the hydrocarbon is 97% of total fuel mass, $m_{fuel} = 9717.4/0.97 = 10{,}017.9\ \text{g}$, so $m_S = 0.03(10{,}017.9) = 300.5\ \text{g}$ and $n_S = 300.5/32.07 = 9.37\ \text{mol}$.
3. Balance the combustion. $$\text{C}_7\text{H}_{13} + 10.25\,\text{O}_2 \rightarrow 7\,\text{CO}_2 + 6.5\,\text{H}_2\text{O}, \qquad \text{S} + \text{O}_2 \rightarrow \text{SO}_2.$$ Required O₂: $100(10.25) + 9.37(1) = 1034.4\ \text{mol}$.
4. Stoichiometric air and its N₂. $n_{air} = 1034.4/0.21 = 4925.6\ \text{mol}$, so $n_{N_2} = 0.79(4925.6) = 3891.2\ \text{mol}$.
5. Total flue gas and SO₂ fraction. $n_{CO_2}=700$, $n_{H_2O}=650$, $n_{SO_2}=9.37$, giving $$n_{flue} = 700+650+9.37+3891.2 = 5250.6\ \text{mol}.$$ $$y_{SO_2} = \frac{9.37}{5250.6} = \boxed{1.78\times10^{-3} \approx 1785\ \text{ppmv}\ (0.18\%)}.$$

Secondary air pollutants from fossil-fuel combustion. Combustion emits primary pollutants directly (SO₂, NOx, CO, unburned hydrocarbons, primary PM), but many of the most damaging species form only afterward, in the atmosphere, from those primary emissions. SO₂ and NOx are oxidized by OH radicals and, in cloud droplets, by dissolved oxidants, to sulfate and nitrate aerosol and to dilute sulfuric/nitric acid, driving acid deposition and a large share of regional PM2.5 mass. Separately, NOx and unburned volatile hydrocarbons react photochemically in sunlight to produce ground-level ozone and photochemical smog (the mechanism detailed in Question 1(iii)). Both pathways mean that reducing only the primary emission at the stack is not the whole air-quality story — secondary chemistry redistributes the impact in both space (downwind) and pollutant identity (SO₂ gas becomes sulfate PM).

(ii) A Biological and a Chemical Air Pollutant in a City Environment

Biological: bioaerosols (mould spores and pollen). In an urban setting these arise both indoors (damp building materials, HVAC condensate pans) and outdoors (urban trees, damp basements venting to alleys); inhalation triggers allergic rhinitis and asthma exacerbation, and in immunocompromised individuals mould spores can cause invasive respiratory infection. Two technical strategies: (1) mechanical ventilation with humidity control (HRV/dehumidification keeping indoor RH below ~60%, the threshold that supports mould growth) and (2) HVAC filtration upgraded to a MERV 13+ filter, which captures the 2–10 µm size range typical of spores and pollen far more effectively than a standard residential filter.

Chemical: ground-level ozone (a secondary photochemical pollutant, Question 1(iii)). Ozone is a strong respiratory irritant that reduces lung function and aggravates asthma/COPD, with measurable effects even at concentrations below historical air-quality objectives during summer smog episodes. Two technical strategies: (1) VOC emission control at the source — low-VOC coatings/solvents and vapour-recovery on fuel dispensing, which starves the radical chemistry that converts NOx to ozone (Question 1(iii)); and (2) NOx control on mobile/stationary sources (catalytic converters, SCR) to limit the other precursor, since ozone formation is jointly limited by both VOC and NOx availability depending on the local VOC/NOx ratio.

(iii) Fugitive Benzene Emission from an Industrial Park

Health impacts. (1) Haematotoxicity and leukaemia risk — benzene is a well-established human carcinogen (IARC Group 1); chronic inhalation is causally linked to acute myeloid leukaemia and other blood dyscrasias because its reactive epoxide metabolites damage bone-marrow stem cells, with no identified safe threshold of exposure. (2) Acute and chronic irritant/neurological effects — short-term exposure causes headache, dizziness and mucous-membrane irritation, while chronic low-level exposure in a residential population near an industrial park is associated with elevated risk even at trace ambient concentrations, which is why benzene is on CEPA's Toxic Substances List.

Ecological impacts. (1) Photochemical precursor role — as a reactive VOC, fugitive benzene contributes to the NOx–VOC–ozone smog cycle (Question 1(iii)), degrading regional air quality and vegetation health (ozone is itself phytotoxic, reducing crop yield and forest growth) well beyond the industrial park boundary. (2) Soil and groundwater contamination pathway — fugitive vapour emissions condense and deposit near the source, and benzene's relatively high water solubility and mobility mean spilled/deposited product can migrate to groundwater, threatening aquatic ecosystems and downgradient wells long after the atmospheric release itself has dispersed.