What does this research mean for the field?

Traffic-related emissions are the primary source of PM2.5-bound PAHs in urban primary schools, leading to indoor carcinogenic risks for children that can exceed standard safety thresholds. Novelty: ClaimNovelty.INCREMENTAL. Consensus alignment: ConsensusAlignment.NEUTRAL.

What question did this study set out to answer?

To evaluate the distribution, emission sources, and health risks of fine particulate matter (PM2.5)-bound polycyclic aromatic hydrocarbons (PAHs) in indoor and outdoor school environments.

August 22, 2026Asian Journal of Atmospheric EnvironmentOpen Access

Unveiling distribution and health risks of polycyclic aromatic hydrocarbons (PAHs) bound to PM2.5 in indoor and outdoor environments of urban primary schools

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Authors

MIMohamad Ismail MFMuhammad Fais Fadzil NNNur Nadrah Mohd Naim

Discussion

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Overview

Observational study reveals traffic-derived particulate PAHs pose indoor carcinogenic risks to school children, highlighting the need for traffic emission controls.

Key Points

To evaluate the distribution, emission sources, and health risks of fine particulate matter (PM2.5)-bound polycyclic aromatic hydrocarbons (PAHs) in indoor and outdoor school environments.
Collected indoor and outdoor PM2.5 samples at urban primary schools using low-volume samplers equipped with quartz fiber filters.
Extracted samples via ultrasonic extraction in dichloromethane/n-hexane (1:1) and analyzed chemical constituents using gas chromatography-mass spectrometry (GC-MS).
Applied diagnostic ratios and principal component analysis (PCA) for source identification, and assessed carcinogenic risks for children aged 7–12 years.
Mean total PAH concentrations were 4.34 ± 2.39 ng m⁻³ indoors and 5.62 ± 2.39 ng m⁻³ outdoors, with high molecular weight five- and six-ring PAHs representing over 60% of totals.
Diagnostic ratios and PCA identified gasoline and diesel traffic emissions as the primary sources of PAH contamination.
Outdoor carcinogenic risk for children aged 7–12 years remained acceptable, but indoor risk levels in certain schools exceeded the standard safety threshold of 10⁻⁶ to 10⁻⁴.

Cite This Study

Ismail et al. (2026) studied this question.

synapsesocial.com/papers/6a895f41ca7ade938187dcd6 https://doi.org/10.1007/s44273-026-00094-3

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August 22, 2026Asian Journal of Atmospheric EnvironmentOpen Access

Unveiling distribution and health risks of polycyclic aromatic hydrocarbons (PAHs) bound to PM2.5 in indoor and outdoor environments of urban primary schools

View Full Paper

Ask AI

Bookmark

Authors

MIMohamad Ismail MFMuhammad Fais Fadzil NNNur Nadrah Mohd Naim

Discussion

Member takes

Overview

Observational study reveals traffic-derived particulate PAHs pose indoor carcinogenic risks to school children, highlighting the need for traffic emission controls.

Key Points

To evaluate the distribution, emission sources, and health risks of fine particulate matter (PM2.5)-bound polycyclic aromatic hydrocarbons (PAHs) in indoor and outdoor school environments.
Collected indoor and outdoor PM2.5 samples at urban primary schools using low-volume samplers equipped with quartz fiber filters.
Extracted samples via ultrasonic extraction in dichloromethane/n-hexane (1:1) and analyzed chemical constituents using gas chromatography-mass spectrometry (GC-MS).
Applied diagnostic ratios and principal component analysis (PCA) for source identification, and assessed carcinogenic risks for children aged 7–12 years.
Mean total PAH concentrations were 4.34 ± 2.39 ng m⁻³ indoors and 5.62 ± 2.39 ng m⁻³ outdoors, with high molecular weight five- and six-ring PAHs representing over 60% of totals.
Diagnostic ratios and PCA identified gasoline and diesel traffic emissions as the primary sources of PAH contamination.
Outdoor carcinogenic risk for children aged 7–12 years remained acceptable, but indoor risk levels in certain schools exceeded the standard safety threshold of 10⁻⁶ to 10⁻⁴.

Cite This Study

Ismail et al. (2026) studied this question.

synapsesocial.com/papers/6a895f41ca7ade938187dcd6 https://doi.org/10.1007/s44273-026-00094-3

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