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Effect of tomato juice on the sperm quality of mice exposed to tertiary cigarette smoke
Published in Ade Gafar Abdullah, Isma Widiaty, Cep Ubad Abdullah, Medical Technology and Environmental Health, 2020
A.R. Furqaani, A.K. Sari, R. Ekowati, L.H. Siswanti, A. Triamullah, T. Sugiartini
Dai and colleagues (2015) have shown that toxins in cigarettes are compounds that play a role in activating the oxidative stress mechanism so that there is an increase in free radicals in the body. This free radical increase is positively correlated with DNA fragmentation and damage. Benzo(a)pyrene (B[a]P) found in cigarette smoke is mutagenic and carcinogenic. The compound will bind with DNA covalently to form a DNA adduct called benzo(a)pyrene diol epoxide-DNA (BPDE-DNA). It is known that BPDE-DNA increases in smokers and significantly decreases the percentage of halo acrosomes and is a contributing factor of DNA damage in smokers’ sperm (Hammadeh et al. 2016). Increasing environmental pollutants, including cigarette residues, expose humans to various substances that threaten health. Therefore, people need to change their lifestyle and consume food and nutrients that can minimize these adverse effects.
The respiratory system
Published in C. Simon Herrington, Muir's Textbook of Pathology, 2020
Asthma occurs in 12%–15% of children, and the incidence has increased by 50% between the mid-1970s and mid-1980s in industrialized countries. The prevalence of eczema and hayfever similarly rose, suggesting an increase in allergy. Similarly, there has been a link to an increase in environmental pollutants. Asthma may be classified as atopic (in patients sensitized to an allergen) or non-atopic (no sensitization).
Mitochondrial Dysfunction and Allergic Disease
Published in Shamim I. Ahmad, Handbook of Mitochondrial Dysfunction, 2019
Kritika Khanna, Anurag Agrawal
Environmental pollutants have been strongly associated with allergic diseases and asthma. There are several studies demonstrating that air borne particulate matter can trigger mitochondrial dysfunction via multiple mechanisms. Exposure of rat lungs to particular matter below 2.5 µm diameter (PM2.5) disrupts mitochondrial dynamics by affecting the expression of proteins regulating mitochondrial fission (dynamin related protein, DRP1) and mitochondrial fusion (optic atrophy protein, OPA1) (Li et al. 2015). Early life exposure of PM is also associated with increased mitochondrial oxidative DNA damage in both mothers and their newborns (Grevendonk et al. 2016). Pollutants like diesel exhaust particles have also been shown to induce mitochondrial dysfunction via increased ROS generation, disruption of mitochondrial membrane potential, release of cytochrome c and subsequent activation of the apoptotic pathway (Wang et al. 2007). Moreover, diesel exhaust particles also decrease the ubiquitin proteasome system which is important for mitochondrial quality control (Kipen et al. 2011). Studies have shown that exposure to other pollutants like cadmium increases lipid peroxidation which induces mitochondrial membrane permeability and release of mitochondrial calcium (Müller 1986). Overall, these studies highlight the effect of air pollutants on mitochondrial function suggesting mitochondria as the common, connecting link between rise in pollution levels and increased prevalence of allergic diseases.
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
It is accepted that environmental pollutants are associated with enhanced risk of pulmonary, cardiovascular disorders and are important causative agents for lung, pancreatic, and prostate cancers (Duca et al. 2018; Marris et al. 2020). According to the World Health Organization (WHO) the countries of the Balkan Peninsula have significantly high mortality rates caused by exposure to organic pollutants, particularly the Republic of North Macedonia which has the fourth highest mortality rate in Europe (WHO 2018). Toxicological studies have identified polycyclic aromatic hydrocarbons (PAH) in human breast milk, smoked and barbequed food, although the largest contribution of PAH intake into the body are cereals and cereals products, followed by barbecued meat and vegetables (Zelinkova and Wenzl 2015; Tfouni et al. 2018). The effects of PAH on human health depend mainly on the length, dose, and route of exposure, including subjective factors such as preexisting health and age. The major effects attributable to PAH appeared to occur in the liver, lungs, the hematopoietic system, and kidney (Kim et al. 2019; Petit et al. 2019).
Early-life exposure to air pollution and childhood allergic diseases: an update on the link and its implications
Published in Expert Review of Clinical Immunology, 2020
Chan Lu, Dan Norbäck, Yuguo Li, Qihong Deng
Although previous studies have shown that environmental factors, such as outdoor air pollution, indoor environmental tobacco smoke (ETS), mold/dampness, allergens, and some chemicals are associated with the development of allergies [39,40], which particular environmental pollutant is the primary factor responsible for the rapid increase of childhood allergies is unknown. China has experienced a serious increase in ambient air pollution concentrations during the past few decades [18]. With rapid economic development and industrialization, together with a coal-dominated energy structure, the levels of industrial air pollution (e.g., SO2) in China are among the highest in the world [41,42]. Traffic emissions are increasing substantially due to the rapidly increasing number of vehicles on the roads [32]. Outdoor air pollution in China is therefore characterized by high concentrations and mixed pollution sources, which differs significantly from that in developed countries [18]. The rapid urbanization, in which a great number of newly married couples and young parents have moved to the cities and become the main residents of new buildings, is thought to be related to the increase in asthma prevalence [43]. New building materials, decoration materials and new furniture can increase the concentration of harmful indoor chemicals, such as volatile- and semi-volatile organic compounds (VOCs, SVOCs) [44]. Women and children tend to be exposed to these indoor environmental pollutants for longer periods of time [45]; however, the health effects due to this indoor exposure remain unclear.
Protective effect of naringin against BPA-induced cardiotoxicity through prevention of oxidative stress in male Wistar rats
Published in Drug and Chemical Toxicology, 2020
Mohammad Javad Khodayar, Heibatollah Kalantari, Masoud Mahdavinia, Layasadat Khorsandi, Soheila Alboghobeish, Azin Samimi, Saeid Alizadeh, Leila Zeidooni
The present study revealed that BPA-induced cardiotoxicity in male Wistar rats through the generation of oxidative stress and naringin protected the heart tissue through suppressing free radicals, increasing antioxidant defense, and decreasing serum lipid. There are multiple factors including genetic factors, lifestyles, and environmental contaminants that can cause cardiovascular diseases. Among them, environmental contaminants have been less taken into account. It has been recently reported that there are relationships between environmental pollutants such as air particulates, persistent organic pollutants, heavy metals, lead (Melzer et al. 2010), arsenic (Ahangarpour 2018) and cardiovascular disease. BPA has been considered as an endocrine disrupting chemical and an environmental pollutant associating with heart diseases. Effects of BPA on cardiovascular system include acute and chronic exposure. Effect of acute BPA exposure causes cardiac arrhythmias following ischemia injury, irreversible cell damage, ventricular dysfunction, and ultimately heart failure according to the impact of BPA on estrogen receptors activation in heart tissue (Grohe et al. 1998; Posnack et al. 2015). Effects of chronic BPA exposure result in the increased systolic, diastolic, and mean arterial pressures, oxidative stress, and inflammation (Ezz et al. 2015; Patel et al. 2015).