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Toxic Responses of the Blood
Published in Stephen K. Hall, Joana Chakraborty, Randall J. Ruch, Chemical Exposure and Toxic Responses, 2020
In the normal person, the natural process termed “auto-oxidation” is believed to account for the steady state small amounts of the 1% methemoglobin in blood. Generally, cyanosis becomes apparent when the methemoglobin concentration exceeds 15%, but most people do not exhibit any symptoms until about 20%. The industrial terms of “blue lip” or “huckleberry pie face” refer to the cyanotic complexion as a result of methemoglobinemia. At levels of about 20 to 70%, depending on the individual, methemoglobin weakness accompanied by dizziness, headaches, tachycardia, or dyspnea may occur. Chemicals can convert hemoglobin to methemoglobin either directly or indirectly. Some of these chemicals are listed in Table 7.2. Direct action is associated with nitrites, chlorates, hydrogen peroxide, hydroxylamine, quinone and methylene blue. Nitrites and nitrates, which are reduced to nitrite by gastrointestinal bacteria, act by destabilizing the oxygen-hemoglobin complex, allowing oxygen itself to oxidize the iron to the Fe3+ state. Methylene blue accomplishes oxidation by acting as a hydrogen donor in the presence of molecular oxygen. In contrast, indirect action occurs with aniline, nitrobenzene, and other amino-, nitro-, and aryl- compounds. These chemicals are active in vivo in the indirect formation of methemoglobin.
Pulmonary complications of illicit drug use
Published in Philippe Camus, Edward C Rosenow, Drug-induced and Iatrogenic Respiratory Disease, 2010
Inhaled nitrites pose the risk of developing significant life-threatening methemoglobinaemia. Methemoglobin is a ferric (Fe3+) oxidized instead of the normal ferrous (Fe2+) state haemoglobin, a poor oxygen carrier. Emergent recognition is warranted. The condition may follow exposure to inhaled nitrites in so-called ‘poppers’, as named from the brisk noise of opening the rubber stopper of nitrite mini-vial. The condition is suspected when slate-grey cyanosis and low pulse O2 saturation (SpO2) develop, along with a normal dissolved PaO2 and calculated SaO2. Multi-wavelength examination of an arterial blood sample is required to quantitate methemoglobin and confirm the diagnosis. Management includes high-flow oxygen, cessation of exposure to the agent, intravenous methylene blue, and in severe cases hyperbaric oxygen therapy.
Toxicology
Published in Martin B., S.Z., of Industrial Hygiene, 2018
In the normal person, the natural process termed “auto-oxidation” is believed to account for the steady-state small amounts of 1% methemoglobin in blood. Generally, cyanosis becomes apparent when the methemoglobin concentration exceeds 15%, but most people do not exhibit any symptoms until about 20%. The industrial terms of “blue lip” or “huckleberry pie face” refer to the cyanotic complexion as a result of methemoglobinemia. At levels of about 20–70%, depending on the individual, methemoglobin weakness accompanied by dizziness, headaches, tachycardia, or dyspnea may ensue.
Protective Properties of Traditional Wood Paint Based on Cattle Blood
Published in International Journal of Architectural Heritage, 2022
Jan Baar, Péter György Horváth, Qinglin Wu, Tomáš Dostál
The treatment of cattle blood-based paint initially gives wood bright red color, as can be seen in Figure 2. Corresponding color parameters values are stated in Table 5. After a week pass the application, all measured color parameters values decreased in both observed recipes. The color became darker and less red and less yellow. In the course of a time the bright brick red color turns to a dark brown color (Figure 2). The oxblood as the color name usually describes dark red hue with purple and brown undertones, which correspond with the appearance of aged paint (Figure 2). Schießl (1981) stated that the initially shiny, bright red color of the painting is becoming brown and unsightly; an almost blackish hue is seen on the oak wood due to high tannin content. The red color of the blood is given by the erythrocytes, which are red due to the presence of hemoglobin, the metalloprotein responsible for oxygen transport. Hemoglobin is composed of four subunits, each composed of a protein chain and a non-protein heme group—an iron ion surrounded by a heterocyclic porphyrin ring. Its oxygenated form is responsible for the typical red color of fresh blood. Hemoglobin, which constitutes 97% of the blood’s dry content when in contact with oxygen outside the living body, is converted to three consecutive derivatives: oxyhemoglobin (bright red), methemoglobin (dark red), and hemichrome (dark brown). The discoloration is the most rapid within the first 10 hours and later the rate slows down; the reaction rate also depends on temperature and humidity (Bremmer et al. 2011).
A time series analysis of ambient air pollution and low birth weight in Xuzhou, China
Published in International Journal of Environmental Health Research, 2022
Jingwen Hao, Lei Peng, Peng Cheng, Sha Li, Chao Zhang, Weinan Fu, Lianjie Dou, Fan Yang, Jiahu Hao
The biological mechanism of how low birth weight might be caused by air pollution is not clear. Several hypotheses suggest that these pollutants directly affect the development of the placenta, resulting in a decline in the mother’s ability to carry oxygen and provide sufficient nutrition to the developing embryo and fetus(Guoqing Zhao 2008). Also, certain pollutants can directly damage fetal development and DNA expression, causing the body to produce numerous free radicals and result in inflammation(Dugandzic et al. 2006). The biological pathways through which air pollutants might act include systemic oxidative stress and inflammation, changes in blood coagulation, changes in endothelial function, and hemodynamics, as well as others(Linmei Zheng 2011). All of these possible mechanisms can affect the placenta and the developing fetus. For example, SO2 can pass through the placenta to the fetus, severely interfering with normal growth and development, and even cause malformations or death of the fetus(Dugandzic et al. 2006). NO2 can enter the blood in the form of nitrite and nitrate, converting hemoglobin to methemoglobin resulting in tissue hypoxia, impeding nutrient and oxygen exchange between the mother and fetus, damaging the fetus, and indirectly increasing the risk of significant adverse outcomes(Estarlich et al. 2011). O3 increases lipid peroxidation and inflammatory factor concentrations in the circulatory system of pregnant women, affecting placental blood circulation and fetal growth.
A GIS-based analysis of intrinsic vulnerability, pollution load, and function value for the assessment of groundwater pollution and health risk
Published in Human and Ecological Risk Assessment: An International Journal, 2022
Yuanyuan Wang, Kang Fu, Han Zhang, Guangyi He, Rui Zhao, Cheng Yang
Water quality and human health are interdependent (Wu and Sun 2016). Arguably, health risk assessment thus qualifies as extension of the social attribute of groundwater pollution risk. In this respect, the HHRA model has been used to quantitatively evaluate the adverse impact of groundwater pollution upon human health (Zhang et al. 2018; Pazhuparambil and Kuriachan 2021). According to the measured groundwater quality from our 36 samples, the concentrations of nitrate, iron, and manganese in some boreholes already exceed the maximum allowable concentration of the National Standard (GB/T14848-2017) limit for class III pollutants (Zhang et al. 2020). A high concentration of nitrate in groundwater could cause adversely affect human health. For example, blue baby disease is caused by the conversion of hemoglobin to methemoglobin due to an excess of nitrate in the body, which consumes a large amount of oxygen in the blood (Gao et al. 2020). Stomach cancer has also been linked to excessive nitrate intake (Kaur et al. 2020). In other cases, high concentrations of manganese can be hazardous to human health. Infants exposed to drinking groundwater high in manganese had a 34% increased risk of death in the first year of life, compared with infants not exposed to manganese levels higher than 0.4 mg/L (Ghosh et al. 2020).