In association with the mortality rate due to air pollution, vehicular emitted fine particles (PM 2.5) are a threat to public health. PM 2.5-induced in-vivo studies on environmental microorganisms can be used to assess the adverse impacts of PM 2.5 on human health. In the present study, the toxicity of traffic-related-air-pollutant (TRAP) PM 2.5 was evaluated in the animal model Caenorhabditis elegans (C. elegans) using different toxicological endpoints such as lethality, survivability (lifespan), behavioral (head thrashing and body bending), and reproduction (brood size). The TRAP PM 2.5 sample were collected in Taichung City, Taiwan from Mar 24 to April 15 in 2018. Of these 23 day samples, three samples (Days A, B, and C) were randomly selected. The results showed that no immediate lethality was observed after acute (24 h) exposure of the nematodes. On the other hand, sublethal endpoints of reproduction exhibited statistically significant dose-dependent reduction, although Day A and Day C did not decrease the egg-laying capability of the worms. For the neurological toxicity, it is inferred that the higher the PM 2.5 concentrations, the more the adverse effects of neurobehavior (head trashing and body bending) it poses on the C. elegans. The lifespans of nematodes exposed to heavily TRAP PM 2.5 were significantly shortened compared with those of untreated ones based on survival rate. The nematodes exposed PM 2.5 models not only posed potentially adverse health effects on human but also represented ecotoxic impacts on the ecosystem. In conclusion, heavy concentrations of TRAP PM 2.5 significantly and severely disrupted toxicological endpoints of neurology and reproduction to C. elegans. TRAP PM 2.5 significantly shortened the lifespan of the nematodes compared with the control. TRAP PM 2.5 might more severely influenced the specific toxic endpoints, such as lifespan and neurobehavira, in this in-vivo models compared with the reproductive endpoints.
Several studies have stated the harmful effects of PM 2.5 to population health, including disruption of neurological development. However, the mechanism behind the neurodevelopmental effects of ambient PM 2.5 and postnatal PBDEs and OCPs exposure is still unknown. Our goal was to determine influence of breastmilk residues, polybrominated diphenyl ethers (PBDEs) and organochlorine pesticides (OCPs), to the infants' neurodevelopment with respect to high and low PM 2.5 exposure areas. The participants were recruited from high PM 2.5 exposure areas (n = 32) and low PM 2.5 exposure areas (n = 23) of southern Taiwan. The extracted 14 PBDEs and 20 OCPs compounds were analyzed using gas chromatography coupled with mass spectrometer. The infants, aging from 8-12 months, were examined by Bayley Scales of Infants and Toddlers Development, Third Edition (Bayley-III) for neurodevelopment. Results showed that high PM 2.5 exposure caused reduced head circumference and had significant effects on the motor skill and social emotional development. For breastmilk PBDEs, a positive correlation between BDE-196 and social emotion, after multivariate analysis with adjustment of confounders, was observed while BDE-99, 196, 197, and 207 showed higher magnitudes in low PM 2.5 areas than in high PM 2.5 areas. For OCPs, only γ-hexachlorcyclohexanes (γ-HCH) presented the significant difference between high and low PM 2.5 exposure areas. Most breastmilk OCPs residues, including 4,4'-dichlorodiphenyltrichloroethane (4,4'-DDT), γ-HCH, endrin, and heptachlor epoxide showed negative impact on the Bayley-III scores after multivariate analysis. In conclusion, infants' neurodevelopment was significantly correlated with the location of PM 2.5 exposure and breastmilk intake of certain PBDEs and OCPs. Breastmilk OCPs might obviously affect infants' neurodevelopment more compared to breastmilk PBDEs based on our finding. Moreover, this study further employs awareness about viable effects of PM 2.5 in infants' neurodevelopment.
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