PM2.5-Bound Polycyclic Aromatic Hydrocarbons and Elements in Different Environments in Southern Taiwan and Their Potential Toxic Effects on Caenorhabditis elegans Models

Abstract Fine particulate matter (PM 2.5 ) has been demonstrated to disrupt developmental, neurological, and reproductive functions in animal models including Caenorhabditis elegans ( C. elegans ). In the present study, PM 2.5 -bound polycyclic aromatic hydrocarbons (PAHs) and elements were studied in urban, traffic-related air pollution (TRAP), and industrial areas to examine whether PM 2.5 -bound PAHs or elements caused toxic effects in C. elegans . PM 2.5 collected from these areas (25.9, 41.7, and 28.9 μg m −3 in urban, TRAP, and industrial areas, respectively) caused significant toxic effects on development (body growth, 85.8%–95.9% reduction), reproduction (brood size, 52.5%–85.8% reduction), and neurology (locomotion, 49.7%–84.3% and 72.3%–94.5% declines in head thrashing and body bending frequencies, respectively), along with changes in the expression of genes regulating antioxidant mechanisms. Despite its lowest PM 2.5 concentration, the industrial site induced stronger reproductive and locomotor toxicity, accompanied by heightened antioxidant gene expression. To further elucidate the role of PM 2.5 composition in these effects, concentrations of PAHs, PAH-BaPeq, and elements were quantified in the nematode exposure models. Our results showed that PM 2.5 -bound Σ 16 PAH (0.501–0.658 ng m⁻ 3 ) and PAH-BaPeq (0.0497–0.0698 ng BaPeq m⁻ 3 ) levels did not differ significantly among the three areas; however, toxic metal concentrations—particularly lead and copper—were substantially higher in the industrial samples than in those from the urban and TRAP environments. The reproductive and locomotor toxicity, along with increased superoxide dismutase (SOD)-related reactive oxygen species (ROS) production observed in nematodes exposed to low-dose industrial PM 2.5 , is likely more strongly associated with elevated levels of PM 2.5 -bound toxic metals than with exposures from urban or TRAP regions. Compared with PM 2.5 -bound PAHs, PM 2.5 -bound lead or copper might contribute more substantially in triggering the toxic responses of PM 2.5 in nematodes, particularly on oxidative stress, reproduction, and locomotion, according to the findings of the current study. Graphical Abstract

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Journal
Aerosol and Air Quality Research
Published
2025-12-01
DOI
https://doi.org/10.1007/s44408-025-00074-2
Primary Topic
Genetics, Aging, and Longevity in Model Organisms
Type
article
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article

PM2.5-Bound Polycyclic Aromatic Hydrocarbons and Elements in Different Environments in Southern Taiwan and Their Potential Toxic Effects on Caenorhabditis elegans Models

Jia-De Lee, Ping-Heng Hsieh, Wan Nurdiyana Wan Mansor, Yi‐Kuo Chang et al.
Aerosol and Air Quality Research
Genetics, Aging, and Longevity in Model Organisms
article

PM2.5-Bound Polycyclic Aromatic Hydrocarbons and Elements in Different Environments in Southern Taiwan and Their Potential Toxic Effects on Caenorhabditis elegans Models

Jia-De Lee, Ping-Heng Hsieh, Wan Nurdiyana Wan Mansor, Yi‐Kuo Chang, How‐Ran Chao, Jen-Hsiung Tsai, Juliana Jalaludin, Chien-Er Huang, Sheng‐Lun Lin, Jian-He Lu, Jheng-Jie Jiang, Tai-Jui Juan
article en

Abstract

Abstract Fine particulate matter (PM 2.5 ) has been demonstrated to disrupt developmental, neurological, and reproductive functions in animal models including Caenorhabditis elegans ( C. elegans ). In the present study, PM 2.5 -bound polycyclic aromatic hydrocarbons (PAHs) and elements were studied in urban, traffic-related air pollution (TRAP), and industrial areas to examine whether PM 2.5 -bound PAHs or elements caused toxic effects in C. elegans . PM 2.5 collected from these areas (25.9, 41.7, and 28.9 μg m −3 in urban, TRAP, and industrial areas, respectively) caused significant toxic effects on development (body growth, 85.8%–95.9% reduction), reproduction (brood size, 52.5%–85.8% reduction), and neurology (locomotion, 49.7%–84.3% and 72.3%–94.5% declines in head thrashing and body bending frequencies, respectively), along with changes in the expression of genes regulating antioxidant mechanisms. Despite its lowest PM 2.5 concentration, the industrial site induced stronger reproductive and locomotor toxicity, accompanied by heightened antioxidant gene expression. To further elucidate the role of PM 2.5 composition in these effects, concentrations of PAHs, PAH-BaPeq, and elements were quantified in the nematode exposure models. Our results showed that PM 2.5 -bound Σ 16 PAH (0.501–0.658 ng m⁻ 3 ) and PAH-BaPeq (0.0497–0.0698 ng BaPeq m⁻ 3 ) levels did not differ significantly among the three areas; however, toxic metal concentrations—particularly lead and copper—were substantially higher in the industrial samples than in those from the urban and TRAP environments. The reproductive and locomotor toxicity, along with increased superoxide dismutase (SOD)-related reactive oxygen species (ROS) production observed in nematodes exposed to low-dose industrial PM 2.5 , is likely more strongly associated with elevated levels of PM 2.5 -bound toxic metals than with exposures from urban or TRAP regions. Compared with PM 2.5 -bound PAHs, PM 2.5 -bound lead or copper might contribute more substantially in triggering the toxic responses of PM 2.5 in nematodes, particularly on oxidative stress, reproduction, and locomotion, according to the findings of the current study. Graphical Abstract

Aerosol and Air Quality ResearchVol. 25(12)
Universiti Putra Malaysia (MY), Chung Yuan Christian University (TW), Kaohsiung Medical University (TW), Universiti Malaysia Terengganu (MY), National Pingtung University of Science and Technology (TW), Kaohsiung Armed Forces General Hospital (TW), Kaohsiung Veterans General Hospital (TW), National Cheng Kung University (TW), Cheng Shiu University (TW)
Openalex Percentile: Top 66%
Genetics, Aging, and Longevity in Model Organisms
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