China
Africa
Explore chapters and articles related to this topic
Inhalation Toxicity of Metal Particles and Vapors
Published in Jacob Loke, Pathophysiology and Treatment of Inhalation Injuries, 2020
Acute toxicity is caused by a relatively large dose of a metal toxicant. The onset of symptoms is sudden, and the intensity of effects rises rapidly and if adequate procedures are not performed to neutralize or remove the toxicant, irreversible damage to tissues and systems may cause death. Chronic poisoning develops gradually following long and continued exposure to relatively small doses. Initially, no symptoms manifest, then there is a gradual onset of symptoms. There may be frequent remissions and recurrences of the symptoms. Many metals act as short-term poisons or toxicants in high doses and as long-term systemic poisons in low doses. Chronic poisoning also represents cumulative effects. A metallic toxicant can develop two different sets of symptoms, one for acute and one for chronic toxicity. Chronic toxicity can be reversed by removal of the toxicant, provided no irreversible damage has been done to vital systems. Groth (1972) found that metal interactions were effective in chronic experiments, with mercury toxicity being alleviated by selenium. Delayed, or latent, toxicity is the condition in which clinical effects are observable only months following exposure to the toxicant. Latent toxicity is exemplified by beryllium and chromium. Cumulative effects may or may not be associated with a build up of the toxicant. For example, there is no cumulative concentration of beryllium in pulmonary tissues in the pulmonary granuloma caused by chronic beryllium toxicity.
Environmental Exposures and Reproduction *
Published in Michele Kiely, Reproductive and Perinatal Epidemiology, 2019
Many environmental studies have used existing data to estimate the study member’s exposures. Some methods of quantifying exposure may include such items as: Usage patterns of a toxicant such as pounds of pesticide used in specific counties and perhaps their seasonal patterns (e.g., see References 22, 25, 31, and 32)Ambient air or water measurements (e.g., see References 23, 26, 27, 33, and 34), distance from a source of pollution (e.g., see References 35 to 40)Environmental monitoring in an individual’s immediate environment such as lead in house dust or in the home’s tap water, toxicants in residential soil/on food (e.g., see References 41 to 43)Biological monitoring of the individual such as blood, urine, or breast milk levels of the toxicant or its metabolites (e.g., see References 41, 42, 44, and 45)
Naturopathic Medicine and the Prevention and Treatment of Cardiovascular Disease
Published in Stephen T. Sinatra, Mark C. Houston, Nutritional and Integrative Strategies in Cardiovascular Medicine, 2015
There is another environmental toxicant that is slowly emerging as a threat to our health, and it is not a heavy metal, chemical, or pesticide.133 This invisible toxin is the increasing expansion and use of wireless technologies that emit radio frequencies. EMR, or wireless radiation, is a frequency that we cannot see, feel, hear, taste, or smell, and as such we do not realize when we are exposed. These devices include cell phones and cell phone antennas, cordless phones, Wi-Fi routers, microwave ovens, smart meters, baby monitors, tablets, computers, and any other device that utilizes wireless technology. Unfortunately, radio frequency devices were not rigorously tested before market release, and some say our safety regulations are obsolete.
Sex differences in the association of measures of sexual maturation to common toxicants: Lead, dichloro-diphenyl-trichloroethane (DDT), dichloro-diphenyl-dichloroethylene (DDE), and polychlorinated biphenyls (PCBs)
Published in Annals of Human Biology, 2021
Casey N. West, Lawrence M. Schell, Mia V. Gallo
Several articles provide accessory information concerning sexual maturation in both boys and girls. For boys’ testicular volume maturation staging, one analysis reports decreased testicular volume for age in association with NDLmPCBs and DDE exposure (Grandjean et al. 2012). Two additional analyses report delays in testicular volume development in association with BLL (Williams et al. 2010; Khalaf et al. 2019). Another analysis found a reduction in testosterone levels of adolescent boys after correction for Tanner stages (Schell et al. 2014). A study of prenatal exposure to polybrominated biphenyls found an acceleration in age at menarche (Blanck et al. 2000). In addition, some studies on sexual maturation also reported hormone levels, which are not the focus of this paper. These findings support the observed disruptions in maturation. In one analysis, oestradiol levels in girls are negatively associated with both PCB and DDT levels (Su et al. 2012). Decreases in free-androgen index levels in girls, as well as a decrease in follicle numbers, are found to be associated with increased sum PCB levels (Kristensen et al. 2016). While these studies are not the focus of this review, they are supporting evidence for disruptions from increased toxicant exposure.
The Toxic Effects of Ethylene Glycol Tetraacetate Acid, Ferrum Lek and Methanol on the Glutathione System: correction Options
Published in Expert Review of Clinical Pharmacology, 2021
Different substances have varying toxicity. Since it manifests itself when a xenobiotic interacts with a biological system, its level depends on the properties of both the toxicant and the biosystem and is ultimately determined by: (1) the ability of the toxic substance to reach a target site; (2) the nature and strength of toxicant–target interaction; (3) and the target’s role in maintaining homeostasis. The structure of the biological system and its morpho-functional organization underwent relatively little change throughout history. Hence, a particular toxic substance with its specific properties will have a unique effect on the organism (biological system). The change of the toxicant will entail qualitative and/or quantitative alterations in that effect. One of the most important principles of toxicology holds that qualitative and quantitative characteristics of toxicity are dependent upon the structure of the toxicant.
Markers involved in proinflammatory effects by environmental toxicants
Published in Toxicology Mechanisms and Methods, 2020
Vesna Smiljevska-Ristovska, Arita Sabriu-Haxhijaha, Trpe Ristoski, Frosina Kosharkoska-Spasovska, Ljupcho Krstanoski, Jasmina Dimitrova-Shumkovska
The DMBA treatments resulted in mild to moderate toxic effects as evidenced by gross anatomical observations of pale and swollen livers, including microscopic observations of a glossy appearance as well as heterochromatic cell nuclei in the liver, evidenced in groups exposed to 20 mg of the toxicant. Vacuolar degeneration of hepatocytes was registered in DR 20 group (Figure 2(c)). The DMBA treatment also provoked glycogen overload which was prominent in the midzonal region of the hepatic lobes (Figure 2(f)). This effect appeared to be dose-dependent (DR20 > DS20). A study by (Muto et al. 2003) reported reversible hepatic toxicity by aromatic hydrocarbons with temporal storage of hepatic glycogen granules suggesting decreased glycogen phosphorylase activity. Other studies have declared similar findings of the effects of carcinogen/toxicant drug and hepatic damage (Zhu et al. 2018; Mohamed et al. 2020). Another study reported a dose-dependent association between furan administration in Fischer F344 rats and perturbations of hepatic gene expression and molecular pathways mainly involved in inflammatory and antioxidant response (Dong et al. 2016).