區域及族群尺度下室內吸入與攝食微型塑膠之人體暴露風險評估

Abstract

微型塑膠廣泛存在於世界各個區域，成為全球關注之環境議題。於各種環境介質中，氣懸微型塑膠易經由吸入途徑進入呼吸道，食源性微型塑膠則易透過食物鏈進入消化系統。多項動物與細胞株研究表明，長期吸入與食入暴露可能導致人體肺部與腸道產生諸多不利影響。然而，目前針對微型塑膠暴露之健康容許值仍缺乏明確制定。 因此，本研究整合人體暴露分析與在生物體內外之毒理學研究資料，評估吸入與食入微型塑膠造成之潛在人類健康風險。吸入暴露是藉由室內粉塵吸入量所推估，而攝食暴露則由飲用水、食鹽、以及魚介類之食用量所推估。於本研究中，利用以生理為基礎團塊肺泡沉積模式與單一團塊腸道毒理動力模式推估肺泡與腸道之微型塑膠累積劑量。並利用希爾模式描述微型塑膠累積劑量與人體細胞氧化壓力、發炎反應、及細胞凋亡之劑量反應關係，再應用韋伯閾值模式推估特定毒性指標其累積劑量閾值。接著，應用機率風險模式進行評量潛在健康風險。此外，基於危害商數推估經由吸入室內粉塵之每日建議微型塑膠暴露量，以及經由食入三類食物之每日微型塑膠參考劑量。 研究結果指出，微型塑膠誘發人體肺部與腸道生物學反應事件之順序為，氧化壓力，接著發炎反應，最後導致細胞凋亡。氣懸微型塑膠暴露於 50% 超越風險下具有較高之氧化壓力增強風險；而食源性微型塑膠暴露則具較高之發炎反應增強風險。而進一步推估不同途徑之每日允許暴露量顯示，經由室內粉塵吸入微型塑膠之平均每日建議暴露量約為 24 至 201 mg kg−1 bw d−1；透過飲用水、食鹽、及魚介類食入微型塑膠之每日參考劑量分別約為 0.3 (中位數，95%信賴區間: 0.03–1.5)、2×10−3 (2×10−4–0.01)、及 0.05 (3×10−3–0.1) mg kg−1 bw d−1。 本研究提出機制性風險評估架構，結合暴露分析、毒理資料、及數理模式，以評量吸入與攝入微型塑膠對呼吸與腸胃系統之潛在危害。而推估之每日建議暴露量，能夠作為未來風險管理與政策發展之科學依據，以減緩微型塑膠對人群造成之潛在健康影響。

Microplastics (MPs) have ubiquitously distributed across global environments, emerging as a critical environmental health concern. Among the environmental media, airborne MPs can enter into the human respiratory system through inhalation, whereas foodborne MPs can be introduced into the gastrointestinal tract through food chain. A growing body of evidence based on animal and cell line studies has revealed that the toxicity of long–term MPs exposure through inhalation and ingestion were highly likely to induce adverse effects in lungs and intestines. However, human healthbased thresholds for MPs exposure still remain inadequately defined. This study integrated human exposure assessment with toxicological data derived from both in–vivo and in–vitro studies to evaluate the potential health risks from inhalation and ingestion of MPs. Inhalation exposure was estimated based on indoor dust intake, whereas ingestion exposure was assessed through consumptions of drinking water, salt, and shellfish. In this study, a compartmental physiologically–based alveolar deposition model and a one–compartmental gastrointestinal tract toxicokinetic model were employed to estimate the cumulative MPs burden in alveoli and intestines, respectively. The Hill–based dose–response model was applied to construct the relationships between MPs accumulation and adverse cellular effect, including oxidative stress, inflammation, and apoptosis. The Weibull threshold model was adopted to estimate toxicity effect–specific thresholds. Subsequently, a probabilistic risk assessment was conducted to evaluate potential health risks. Moreover, hazard quotient–based estimates were used to derive recommended daily intakes (RDI) for inhalation and reference doses (RfD) for ingestion exposure pathways. The results indicated a sequential pattern of adverse effects induced by MPs accumulation, beginning with oxidative stress, followed by inflammation, and subsequent apoptosis. Under exceedance risk of 50%, exposures to airborne MPs resulted in a more pronounced percentage increase in oxidative stress, whereas foodborne MPs exposures were associated with a greater increase in inflammatory responses.The results also showed that the average RDI for inhaled MPs through indoor dust ranged from ~ 24 to ~ 201 mg kg−1 bw d−1. The derived RfDs for ingested MPs were ~ 0.3 (median, 95% CI: 0.03–1.5), ~ 2×10−3 (2×10−4–0.01), and ~ 0.05 (3×10−3–0.1) mg kg−1 bw d−1 for drinking water, salt, and shellfish, respectively. This study proposes a mechanistic risk assessment framework that integrates exposure assessment, toxicological data, and mathematical models for assessing the potential health effects of inhaled and ingested MPs on the respiratory and gastrointestinal systems. The recommended daily exposure estimates can be served as a scientific basis for future risk management strategies and policy development, aiming to mitigate the potential health impacts of MPs on human populations.