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Real-world emission factors for different vehicle types and their contributions to roadside air pollution are needed for air-quality management. Tunnel measurements have been used to estimate emission factors for several vehicle types using linear regression or receptor-based source apportionment. However, the accuracy and uncertainties of these methods have not been sufficiently discussed. This study applies four methods to derive emission factors for different vehicle types from tunnel measurements in Hong Kong, China: (1) simple linear regressions (SLR); (2) multiple linear regressions (MLR); (3) positive matrix factorization (PMF); and (4) EMission FACtors for Hong Kong (EMFAC-HK). Separable vehicle types include those fueled by liquefied petroleum gas (LPG), gasoline, and diesel. PMF was the most useful, as it simultaneously seeks source profiles and source contributions. Diesel-, gasoline-, and LPG-fueled vehicle emissions accounted for 52%, 10%, and 5% of PM2.5 mass, respectively, while ammonium sulfate (~20%), ammonium nitrate (6%), and road dust (7%) were also large contributors. MLR exhibited the highest relative uncertainties, typically over twice those determined by SLR. EMFAC-HK has the lowest relative uncertainties due to its assumption of a single average emission factor for each pollutant and each vehicle category under specific conditions. The relative uncertainties of SLR and PMF are comparable. [ABSTRACT FROM AUTHOR]

On-road vehicular emissions were measured in a Hong Kong roadway tunnel and compared to those from a mobile emission model (EMFAC-HK) for the 2003 and 2015 fleets to assess emission changes and effectiveness of emission controls. EMFAC-HK results compared well with tunnel measurement for the 2015 fleet with differences ≤50% for most pollutants. Both measurement and modeled estimates show that non-methane hydrocarbon (NMHC) and PM 2.5 decreased by over 40% from 2003 to 2015. Tunnel measurements also show that nitrogen dioxide (NO 2) and liquefied petroleum gas (LPG) -related NMHC emissions increased due to expanded installation of diesel oxidation catalysts and LPG fueling. Motorcycles and LPG-fueled public light buses (3.7% of the fleet) contributed disproportionally high fractions of carbon monoxide (CO; 27%) and NMHC (49%) and deserve additional emission controls. Fuel economy improvements did not result in expected carbon dioxide (CO 2) emission reductions, indicating that more aggressive CO 2 reductions, particularly from heavy-duty vehicles, are needed. [Display omitted] • Emission model estimates for the 2015 Hong Kong fleet differed by <50% from tunnel measurements for most pollutants. • Vehicle NMHC and PM 2.5 emissions decreased by over 40% from 2003 to 2015. • CO 2 emissions did not decrease as anticipated by improved vehicle fuel economy. • Fleet-average NO 2 /NO x emission ratios increased from 6.7% in 2003 to 14.4% in 2015. • Motorcycles and LPG light buses are disproportionally high CO and NMHC emitters. [ABSTRACT FROM AUTHOR]

Associations between human exposures to vehicular emissions (VE) and cardiopulmonary diseases have been found, with a dearth of information on particle cytotoxicity. This study exposes human lung alveolar epithelial (A549) cells to PM 2.5 (particulate matter with aerodynamic diameter <2.5 μm) samples collected in a tunnel and investigates the oxidative and inflammatory responses. The cytotoxicity factor (CF) is used to normalize the VE cytotoxicity. The emission factors (EFs) were 27.2 ± 12.0 mg vehicle−1 km−1 for PM 2.5 and 4.93 ± 1.67 μg vehicle−1 km−1 for measured polycyclic aromatic hydrocarbons (PAHs). Higher EFs were found for high (4–6 rings) than low (2–3 rings) molecular-weight particulate PAHs. PM 2.5 VE caused oxidative stress and inflammation of human lung cells. Organic carbon (OC), element carbon (EC), and several PAHs were significantly (p < 0.05) correlated with bioreactivity. Higher CFs were found when diesel vehicle counts were highest during the morning rush hour, implying that diesel-fueled VE were major contributors to cytotoxic effects. This study provides a broader understanding of the toxicity in an engine-exhaust dominated environment. • Vehicle emissions cause oxidative and inflammatory responses in human lung cells. • Increased cytokines are related to vehicle-emitted polycyclic aromatic hydrocarbons. • A vehicle cytotoxicity emission factor is derived. • Diesel-fueled vehicles are the major contributors to the cytotoxic effects. This study evaluates the oxidative and inflammatory responses from PM 2.5 samples collected in a traffic dominated Hong Kong tunnel. [ABSTRACT FROM AUTHOR]