In the present study, a series of laboratory experiments were conducted to examine the impact of pyrolysis temperature on the outcome yields of waste coconut shells in a fixed bed reactor under varying conditions of pyrolysis temperature, from 400 to 800 °C. The temperature was increased at a stable heating rate of about 10 °C/min, while keeping the sweeping gas (Ar) flow rate constant at about 100 mL/min. The bio-oil was described by Fourier transform infrared spectroscopy (FTIR) investigations and demonstrated to be an exceptionally oxygenated complex mixture. The resulting bio-chars were characterized by elemental analysis and scanning electron microscopy (SEM). The output of bio-char was diminished pointedly, from 33.6% to 28.6%, when the pyrolysis temperature ranged from 400 to 600 °C, respectively. In addition, the bio-chars were carbonized with the expansion of the pyrolysis temperature. Moreover, the remaining bio-char carbons were improved under a stable structure. Experimental results showed that the highest bio-oil yield was acquired at 600 °C, at about 48.7%. The production of gas increased from 15.4 to 18.3 wt.% as the temperature increased from 400 to 800 °C. Additionally, it was observed that temperature played a vital role on the product yield, as well as having a vital effect on the characteristics of waste coconut shell slow-pyrolysis.

Microplastics (MPs), small plastic particles resulting from the degradation of larger plastic items and from primary sources such as textiles, engineered plastic pellets, etc., have become a ubiquitous environmental pollutant. As their prevalence in the natural environment grows, concerns about their potential impacts on human health have escalated. This review discusses current research findings on the presence of MPs in organs such as the liver, blood, heart, placenta, breast milk, sputum, semen, testis, and urine, while also exploring plausible mechanisms of translocation. Furthermore, the review emphasizes the importance of understanding the potential toxicological effects of MPs on various physiological processes within these organs and their broader implications for human health. This review also examines the pathways through which MPs can enter and accumulate in human organs and bodily fluids, shedding light on the intricate routes of exposure and potential health implications. It is worth noting that the invasive medical procedures may permit direct access of MPs to the bloodstream and tissues, serving as a potential contamination source. However, it is evident that a comprehensive understanding of MPs’ invasion into human organs is vital for effective mitigation strategies and the preservation of both human health and the environment.

The development of nanotechnology has spurred concerns about the health effects of exposure to nanoparticles (NPs) and ultrafine particles (UFPs). Toxicological data on NPs and UFPs may provide evidence to support the development of regulations to reduce the risk of particle exposure. We tried to provide fundamental data to determine differences in cytotoxicity induced by ambient UFPs and engineered metal oxide NPs (ZnO, NiO, and CeO2). UFPs were sampled by using of a nano micro-orifice uniform deposit impactor. Physicochemical characterization of the UFPs and nano metal oxide particles were studied by scanning electron microscopy and transmission electron microscopy. Cellular toxicity induced by the different particles was assessed by using of comprehensive approaches and compared after A549 cells were exposured to the particles. All of the measured particles could damage A549 cells at concentrations ranging from 25 to 200 μg/mL. The lowest survival ratio and the highest lactate dehydrogenase level were caused by nano-ZnO particles, but the highest levels of intracellular reactive oxygen species (ROS) and percentages of apoptosis were observed in cells treated with the soluble fraction of ambient fine particles (PM1.8) at 200 μg/mL. Relatively high concentrations of anthropogenic metals, including Zn, Ni, Fe, and Cu, may be responsible for the higher toxicity of fine ambient particles compared with the ambient coarse particles and UFPs. The selected heavy metals (Zn, Ni, Fe, and Cu) were found to be located in the perinuclear and cytoplasmic areas of A549 cells. The distribution pattern of metals from ambient particles showed that distributions of the metals in A549 cells were not uniform and followed the pattern Cu > Zn > Fe > Ni, suggesting that Cu was absorbed by A549 cells more easily than the other metals. Metal nanoparticles oxides and UFPs at low concentration could damage to cells, but the manufactured metal oxide nanoparticles are not highly toxic to lung cells compared to environmental particles. The local concentration effect of heavy metals in A549 cells, as well as the induction of oxidative stress by the particles, may be responsible for the damage observed to the cells.

Acellular assays of oxidative potential (OP) induced by ambient particulate matters (PMs) are of great significance in screening for toxicity in PMs. In this review, several typical OP measurement techniques, including the respiratory tract lining fluid assay (RTLF), ascorbate depletion assay (AA), dithiothreitol assay (DTT), chemiluminescent reductive acridinium triggering (CRAT), dichlorofluorescin assay (DCFH) and electron paramagnetic/spin resonance assay (EPR/ESR) are discussed and their sensitivity to different PMs species composition, PMs size distribution and seasonality is compared. By comparison, the DTT assay tends to be the preferred method providing a more comprehensive measurement with transition metals and quinones accumulated in the fine PMs fraction. Specific transition metals (i.e., Mn, Cu, Fe) and quinones are found to contribute OP^DTT directly whereas the redox properties of PMs species may be changed by the interactions between themselves. The selection of the appropriate OP measurement methods and the accurate analysis of the relationship between the methods and PM components is conducive to epidemiological researches which are related with oxidative stress induced by PMs exposure.