There are several environmental and human health impacts if human hair waste is not adequately disposed of. In this study, pyrolysis of discarded human hair was carried out. This research focused on the pyrolysis of discarded human hair under controlled environmental conditions. The effects of the mass of discarded human hair and temperature on bio-oil yield were studied. The proximate and ultimate analyses and calorific values of disposed of human hair, bio-oil, and biochar were determined. Further, chemical compounds of bio-oil were analyzed using a gas chromatograph and a mass spectrometer. Finally, the kinetic modeling and behavior of the pyrolysis process were characterized through FT-IR spectroscopy and thermal analysis. Based on the optimized mass of disposed of human hair, 250 g had a better bio-oil yield of 97% in the temperature range of 210-300 °C. The different parameters of bio-oil were: pH (2.87), specific gravity (1.17), moisture content (19%), heating value (19.34 MJ/kg), and viscosity (50 CP). C (56.4%), H (6.1%), N (0.16%), S (0.01%), O (38.4%), and Ash (0.1%) were discovered to be the elemental chemical composition of bio-oil (on a dry basis). During breakdown, the release of different compounds like hydrocarbons, aldehydes, ketones, acids, and alcohols takes place. According to the GC-MS results, several amino acids were discovered in the bio-oil, 12 abundant in the discarded human hair. The FTIR and thermal analysis found different concluding temperatures and wave numbers for functional groups. Two main stages are partially separated at about 305 °C, with maximum degradation rates at about 293 oC and 400-4140 °C, respectively. The mass loss was 30% at 293 0C and 82% at temperatures above 293 0C. When the temperature reached 4100C, the entire bio-oil from discarded human hair was distilled or thermally decomposed.
Zoonosis-based epidemics are inevitable unless we revisit our relationship with the natural world, protect habitats, and regulate wildlife trade, including live animals and non-sustenance products. To prevent future zoonoses, governments must establish effective legislation addressing wildlife trade, protection of habitats, and reduction of the wildlife-livestock-human interface.
Potentially carcinogenic compounds may cause cancer through direct DNA damage or through indirect cellular or physiological effects. To study possible carcinogens, the fields of endocrinology, genetics, epigenetics, medicine, environmental health, toxicology, pharmacology and oncology must be considered. Disruptive chemicals may also contribute to multiple stages of tumor development through effects on the tumor microenvironment. In turn, the tumor microenvironment consists of a complex interaction among blood vessels that feed the tumor, the extracellular matrix that provides structural and biochemical support, signaling molecules that send messages and soluble factors such as cytokines. The tumor microenvironment also consists of many host cellular effectors including multipotent stromal cells/mesenchymal stem cells, fibroblasts, endothelial cell precursors, antigen-presenting cells, lymphocytes and innate immune cells. Carcinogens can influence the tumor microenvironment through effects on epithelial cells, the most common origin of cancer, as well as on stromal cells, extracellular matrix components and immune cells. Here, we review how environmental exposures can perturb the tumor microenvironment. We suggest a role for disrupting chemicals such as nickel chloride, Bisphenol A, butyltins, methylmercury and paraquat as well as more traditional carcinogens, such as radiation, and pharmaceuticals, such as diabetes medications, in the disruption of the tumor microenvironment. Further studies interrogating the role of chemicals and their mixtures in dose-dependent effects on the tumor microenvironment could have important general mechanistic implications for the etiology and prevention of tumorigenesis.
Lifestyle factors are responsible for a considerable portion of cancer incidence worldwide, but credible estimates from the World Health Organization and the International Agency for Research on Cancer (IARC) suggest that the fraction of cancers attributable to toxic environmental exposures is between 7% and 19%. To explore the hypothesis that low-dose exposures to mixtures of chemicals in the environment may be combining to contribute to environmental carcinogenesis, we reviewed 11 hallmark phenotypes of cancer, multiple priority target sites for disruption in each area and prototypical chemical disruptors for all targets, this included dose-response characterizations, evidence of low-dose effects and cross-hallmark effects for all targets and chemicals. In total, 85 examples of chemicals were reviewed for actions on key pathways/mechanisms related to carcinogenesis. Only 15% (13/85) were found to have evidence of a dose-response threshold, whereas 59% (50/85) exerted low-dose effects. No dose-response information was found for the remaining 26% (22/85). Our analysis suggests that the cumulative effects of individual (non-carcinogenic) chemicals acting on different pathways, and a variety of related systems, organs, tissues and cells could plausibly conspire to produce carcinogenic synergies. Additional basic research on carcinogenesis and research focused on low-dose effects of chemical mixtures needs to be rigorously pursued before the merits of this hypothesis can be further advanced. However, the structure of the World Health Organization International Programme on Chemical Safety 'Mode of Action' framework should be revisited as it has inherent weaknesses that are not fully aligned with our current understanding of cancer biology.