Occurrence and risk assessment of phthalic acid esters in drinking water system and investigation of developmental toxicity for early life stage zebrafish

Abstract

Phthalic acid esters (PAEs) are a series of plasticizer that have been widely used into plastic films, wire, perfume, and personal care products. PAEs could be released as emerging contaminants into the environment during the production, transportation, and consumption of the plastic products. In this study, the occurrence, distribution, and ecological risk of PAEs in the urban drinking water supply system were investigated. The concentrations of PAEs in the source water and sediment samples of Shenzhen ranged 0.2–7.4 μg L−1 (mean: 1.3 μg L−1) and 9.2–9594.1 ng g−1 (mean: 847.5 ng g−1), respectively. Di-n-butyl phthalate (DBP), bis(2-ethylhexyl) phthalate (DEHP) were the predominant congeners, accounting for 57.2% in water samples and 94.1% in sediment samples. The hazard quotient (HQ) levels ranged 0.01-0.20, thereby indicating moderate risks of PAEs in the samples. Screening and prioritizing PAEs in drink water system is crucial to the water quality and human health. According to the related consumption and production, 16 PAEs were screened as the candidates for investigation of tap water. The ATSDR method and analytic hierarchy process (AHP) were applied accounting for the occurrence, persistence, bioaccumulation, acute toxicity, chronic toxicity, and long-term human health effects of the PAEs. The QSAR-ICE-SSD model was firstly applied to derive the HQs in effect assessment. The results showed that DBP and DEHP received high scores in both assessment methods. Diisobutyl phthalate (DiBP), the substitutes of DBP, also received relatively high scores, suggesting that DiBP also would attract public concerns. Certain PAEs are often detected in different environmental matrices but related toxicity data are still lacking to support their risk assessment. In the work, the acute toxicities of DiBP and di-n-octyl phthalate (DNOP) were studied using 6 Chinese resident aquatic organisms from 3 phyla and 6 species. The lethal concentration 50% (LC50) ranges of DiBP and DNOP are 4.89–21.45 mg L−1 and 1.45–1200 mg L−1, respectively. The derived acute and chronic predicted no-effect concentrations (PNECs) based on the lognormal model are 0.54 and 0.04 mg L-1 for DiBP and 0.23 and 0.05 mg L-1for DNOP, respectively. DBP and DiBP have been widely used, their toxicity is still largely unknown. The present study was conducted to obtain base data to compare DBP and DiBP for their acute toxicity and joint toxicity, as well as the thyroid hormone levels in exposed zebrafish larvae. The transcripts of hypothalamic-pituitary-thyroid (HPT) axis related key genes were also investigated in zebrafish developing larvae. The LC50 of DBP and DiBP to zebrafish for 96 h are 0.55 mg L-1 and 1.1 mg L-1, respectively. The joint toxicity effect of DBP–DiBP (0.25 mg L-1–0.53 mg L-1) showed a synergistic toxicity effect. Thyroid hormones (THs) levels increased with exposure to 10 μg L-1 of DBP and 50 μg L-1 of DiBP, and both exposures significantly increased the thyroid gland-specific transcriptions of thyroglobulin gene (tg), hyronine deiodinase (dio2) and transthyretin (ttr), indicating an adverse effect associated with the HPT axis. Thus, DiBP, with the same toxicity effect as DBP, still pose environmental risks.