Human health and environmental pollution             No Of Abstract is : 10  
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Association between exposure to pesticides and disorder on hematological parameters and kidney functions in male agricultural workers   
  Nagah M. A. Hassanina,*, O. M. Awadb, S. A. El-Fikib, R.A. I. Abou-Shanaba, R. A. Amera   
  aCity of Scientific Research and Technology Applications, New Borg El Arab City, Alexandria, 21934, Egypt, bHigh Institute of Public Health, University of Alexandria, Egypt    
  nagah_moh2003@yahoo.com   
 
Pesticides occupy critical position among many chemicals to which man can be exposed, their diffusion into the environment cause killing and damaging some forms of life . The lack of highly selective pesticides action represents a risk both for man and other desirable forms of life present in the environment The present study was designed to evaluate the relation between exposure to pesticides and disorder in some hematological parameters and kidney functions of male agricultural workers with mean age (37.11±9.3). One hundred males matched for age and socio economic status were recruited as a control to compare levels of hemoglobin, hematocrit, red blood cell (RBCs), the mean corpuscular volume (MCV), mean corpuscular hemoglobin (MCH), the mean corpuscular hemoglobin concentration (MCHC), and urea and creatinine concentration. The results indicate that there was no significant difference in hemoglobin concentration and hematocrit value among exposed group as compared to control group. However there was a significant decrease (P<0.05) in the RBCs count and a highly significant increase (P<0.01) in MCV among exposed group. There was no significant difference in MCH and MCHC among exposed group. There was a significant increase (P<0.05) in urea (39.4±22 mg/dl) among exposed group as compared to control (35.7±26.3 mg/dl). Also there was a highly significant increase (P<0.01) in creatinine among exposed group (0.953±0.3 mg/dl) as compared to control (0.8±0.2 mg/dl). In conclusion, exposure to pesticides produced a variety of hematological parameters disorder as well as kidney malfunction in human.      

 
Human health and environmental pollution   
  Mrs. Husnia Bassiouny   
  Outpatient Clinic Nursing, Tanta University Hospital    
  husniaelafify123@gmail.com   
 
Environment is the sum total of conditions that surrounds us at a given point of time and space. Environmental pollution any undesirable change in physical , chemical biological characteristics of air , land , water or soil that is likely to have an adverse effect on the natural environment or life . Environmental pollution is reaching worrying proportions worldwide. Urbanization and industrialization along with economic development have led to increase in energy consumption and waste discharges. The global environmental pollution AIR, water,food,land pollution and waste management is considered as international public health problems. Environmental pollutants have various adverse health effects from early life some of the most important harmful effects are perinatal disorders, infant mortality, respiratory disorders, allergy, malignancies, cardiovascular disorders, increase in stress oxidative, endothelial dysfunction, mental disorders, and various other harmful effects . Though, short-term effects of environmental pollutants are usually highlighted, wide range of hazards of air pollution from early life and their possible implication on chronic non-communicable diseases of adulthood should be underscored. Therefore it is time to take action and control the pollution. Otherwise, the waste products from consumption, heating, agriculture, mining, manufacturing, transportation, and other human activities will degrade the environment. Based on the strength of the scientific knowledge regarding the adverse health effects of environmental pollution and the magnitude of their public health impact taken into account. In addition to industrial aspects, the public awareness should be increased in this regard      

 
In vivo assessment of acute, subacute and subchronic hepatotoxicity of crude cyanotoxins of Nile River Nostoc sp   
  Marwa Abu-Serie1, Nermine Nasser1, Abeer Abdel Wahab1, Rehab Shehawy2, Nahed Baddour3, Ranya Amer1   
  1 City for Scientific Research and Technology Applications (SRTACity), New Borg El Arab, Alexandria, Egypt 2 IMDEA-Agua, C/Punto Net 4, Alcalá de Henares, Madrid, Spain 3 Faculty of Medicine, Alexandria University, Egypt    
  marwaelhedaia@gmail.com   
 
The Nile River Nostoc sp. is one of the most widely distributed cyanobacterial genera that produces potentially protein phosphatase (PP) inhibitor; microcystins (MCs). MCs have posed a worldwide concern due to predominant hepatotoxicity to human health. Nostoc was found to produce MC-leucine arginin (MC-LR) which is the highest toxic MC. In this study, we evaluated acute, subacute and subchronic hepatotoxicity of crude MCs toxin of Nostoc sp. through the oral injection of 0.12-80 mg (once), 0.22 mg (once) and 0.002 mg/ kg b.w. (daily for four months) into Albino mice, respectively in comparison with mice received WHO guideline dose of MC. Several parameters were determined including activities of hepatic PP, liver transaminases (ALT and AST), lactate dehydrogenase (LDH), total cholesterol, triglyceride, lipid peroxidation, nitric oxide, index of DNA fragmentation and TNF-α levels as well as liver histopathology. Our results demonstrated that LD50 value of crude toxins of Nostoc was equivalent to 30.23 mg MCs. The subacute and subchronic dose of crude MCs caused hepatotoxicity that may be attributed to PP inhibition, a significant increase of hepatic damage biomarkers (ALT, AST and LDH) and lipid accumulation. MCs induced hepatic oxidative damage that may lead to DNA fragmentation and production of proinflammatory cytokine (TNF-α). As illustrated from the histopathological study, crude MCs of Nostoc sp. show severe collapse in cytoskeleton with subsequent focal degeneration of hepatocytes, inflammation and steatosis. The grade of hepatoxicity in subacute group was higher than that in the subchronic group and WHO group, respectively.      

 
Pollution, mental health and neuroplasticity   
  Prof. Ehab Ramadan   
  NeuroPsychiatry Department, Faculty of Medicine, Tanta University, Egypt    
  ehab_ramadan@yahoo.com   
 
Research indicates that living in areas of high pollution has serious long term health effects. Living in these areas during childhood and adolescence can lead to diminished mental capacity and an increased risk of brain damage. People of all ages who live in high pollution areas for extended periods place themselves at increased risk of various neuropsychiatric disorders. The ability of pollutants to affect the neurophysiology of individuals after the structure of the CNS has become mostly stabilized is an example of negative neuroplasticity. Air pollution is known to affect small and large blood vessels throughout the body affecting also vascular structures in the brain, air pollution can have serious effects on neural functioning and neural matter. In dogs air pollution shows to cause damage to the CNS by altering the blood–brain barrier, causing neurons in the cerebral cortex to degenerate, destroying glial cells found in white matter, and by causing neurofibrillary tangles. These changes can permanently alter brain structure and chemistry, resulting in various impairments and disorders. Neuroinflammation is associated with increased rates of neurodegeneration. Inflammation tends to increase naturally with age. By facilitating inflammation, pollutants such as air particulates and heavy metals cause the CNS to age more quickly. Consequences on mental health, cognition and emotions will be discussed      

 
Comparative Study between Ginkgo biloba and Green tea Administration on Bisphenol A-Induced Cognitive Deficits in Male Albino Rats   
  1Manar M. El Tabaa, M.Sc.; 2Samia S. Sokar, Ph.D.; 3Ehab S. Ramdan, Ph.D.; 4 Inas Z. Abd El Salam, Ph.D. and 5Anis Zaid, Ph.D.   
  1,4Environmental Studies & Research Institute (ESRI), University of Sadat City, Egypt, 2Pharmacology and Toxicology Department, Faculty of Pharmacy, Tanta University, Egypt, 3 Psychiatry Department, Faculty of Medicine, Tanta University, Egypt, 5Pathology Department, Faculty of Veterinary Medicine, University of Sadat City, Egypt    
  manar.eltabaa@esri.usc.edu.eg   
 
Bisphenol a (BPA), an environmental contaminant, can penetrate the blood–brain barrier resulting in cognitive deficits such as learning and memory impairment. Among the herbal remedies that have been proved scientifically as neuroprotective agents, were Ginkgo biloba (Gb) and Green tea (Gt). Therefore, this study was designed to compare between the possible cognitive enhancing properties of (Gb) and (Gt) against BPA-induced cognitive dysfunction in rats .Animals were divided into six groups (10 rats each) and treated daily by an oral gavage for 8 weeks. Vehicle group I (6.25 ml corn oil /kg b.wt. /day); BPA-exposed group II (250 mg BPA /kg b.wt./day); Gb group III (4 mg Gb /kg b.wt./day); Gt group IV (3.6 ml Gt /kg b.wt./day); Gb co-administration group V (Gb 30 min before BPA administration) and Gt co-administration group VI (Gt 25 min before BPA administration). Cognitive functions were assessed using Y-maze Task, Morris water maze (MWM) test and by estimating hippoicampal adiponectin and markers of oxidative stress. Both BPA-exposed and Gt co-administration groups were found to impair learning and memory performance significantly in the terms of decreased the cognitive ability, spatial navigation task, adiponectin level and SOD activity and increased MDA level in hippocampus. In histopathologic examination, Gb co-administration group protected against the recorded pathological changes in hippocampus. In conclusion, the co-administration of Gb potential to reverse cognitive dysfunction and oxidative stress induced by BPA exposure in rats.      

 
Premenstrual Tension Syndrome Influenced by Obesity and Extended Period of Hot Climate Annually in Egypt   
  Samia A El Dardiry 1 , Samer M Zahran 2 , Sherin R Shafik1a, Hisham Salim 3 , Nawal A El Dardiry3   
  1Department of Medical Biochemistry & 1aPhD from Medical Biochemistry, Faculty of Medicine, Tanta University 2Department of Pharmacology, Faculty of Pharmacy, Pharos University 3Department of Obstetrics & Gynecology, Faculty of Medicine, Tanta University    
  abdelhamidragabshafik@gmail.com   
 
Premenstrual tension may become potentiated by life style induced obesity & impact of hot climate alongside monoaminergic neurotransmitter changes which may induce further dysphoric disorders. The study aimed to monitor the psychosomatic manifestations linked to neuroendocrine induced oxidative stress in obese female subjects complaining from premenstrual tension syndrome (PMS). The study focused on monitoring in PMS cases multifacet dynamic change influenced by dual effect of obesity and extended period of hot climate. Sixty selected female middle aged subjects were classified into 30 cases with PMS involving 15 obese cases (Group I) and 15 non obese cases (Group II). Also 30 cases without PMS involving 15 obese (GIII) & 15non obese (GIV) cases were compared . Assessed biochemical indices of induced adipocytokines (Leptin) and interleukin-8 & intracellular adhesion molecule-1 and antioxidant status (vitamin E, glutathione peroxidase, glutathione, malonedialdehyde ) . Their relative impact on heat shock protein 70 & anti-HSP-70 antibody was determined relative to neurotransmitter levels of epinephrine, norepinephrine, dopamine and catabolic enzymes monoamine oxidase & catechol-O-methyl transferase., The results identified relative incriments of leptin, IL-8, ICAM-1 HSP-70 , anti HSP-Ab potentiated by obesity & hot climate associated with decreased antioxidant defense and increased neuroendocrinologic induced psychosomatic changes. It may be concluded that targeted therapy of PMS should focus on alleviating stress related interaction between HSP-70 ,Anti HSP Ab, adipocytokines, oxidative stress and neurotransmitter variations which could influence psychological balance that affects the neurobiology of depression and enhance capability to cope with environmental induced pathophysiological stressors.      

 
Epithelial polarity and integrity as a novel target for asthma therapy   
  Ahmed HK El-Hashash, PhD   
  Assistant Professor & Principal Investigator of Stem Cells & Regenerative Medicine, Keck School of Medicine and Ostrow School of Dentistry, University of Southern California, and Children’s Hospital Los Angeles, 4650 Sunset Blvd., Hollywood, Los Angeles, CA 90027, USA    
  hashash05@yahoo.co.uk   
 
Asthma and bronchitis are epidemic that disproportionately affect children and the poor groups worldwide. The prevalence of asthma/ bronchitis in the Middle East is among one of the highest in the world. Air pollution represents an important cause of exacerbations of asthma/ bronchitis and a major risk factor for respiratory mortality in the Middle East. Zinc and Vanadium (V) are present in several environmental settings, for example, during overhauling of oil-fired boilers and burning of heavy fuel in power plants. Exposures to high levels of Zinc- or V-rich particles produce upper/lower respiratory symptoms. Yet, the molecular mechanisms of Zinc or Vanadium-induced asthma/bronchitis are not fully understood. Disruption of apical-basal polarity results in loss of tight junction barrier integrity/function. This leads to loss of epithelial tissue organization, which is a characteristic feature of asthma. Proper control of cell polarity and barrier integrity/function is critical for being protective against asthma. Yet, whether asthma is due to a primary defect in epithelial polarity and integrity is unknown. Nor do we understand whether cell polarity-regulatory mechanisms can protect against asthma. In this presentation, we will discuss our new hypothesis that asthma is due to a primary epithelial defect in cell polarity and barrier integrity. We will also discuss our preliminary data on novel molecular mechanisms by which protein phosphatases may function to protect against asthma development/exacerbations by maintaining proper epithelial polarity and barrier integrity/function, probably by controlling the activity levels of protein kinases.      

 
Role on Stress Pathways in Reversing Nanomaterial-Induced Cell Death in Human Alveolar Epithelial Cells   
  Punit Kaur1,2,3 and Alexzander A. A. Asea3   
  1 Department of Microbiology, Biochemistry & Immunology, Morehouse School of Medicine, 720 Westview Avenue, SW, Atlanta, GA 30310 USA 2 Department of Radiation Oncology, University of Texas MD Anderson Cancer Center 1515 Holcombe Blvd, Houston, TX 77030 USA 3 Department of Neuroscience Research and the Deanship for Scientific Research, University of Dammam, Al-Rakah 31441 Saudi Arabia    
  aaasea@uod.edu.sa   
 
To understand the health effects of nanomaterials, a better understanding of how it modulates biological functions in vitro and in vivo related to stress and apoptosis must first be understood. This study was designed to determine the toxic effects of collected nanomaterials on human alveolar epithelial cells (HAEC) and mice inoculated with collected nanomaterials. We demonstrate that nanomaterials are toxic to lung tissue via a pathway dependent on stress proteins. We show that administration of nanomaterials to HAEC stimulates a slight activation of stress proteins, including heat shock protein 27 (Hsp27) and heat shock protein 72 (Hsp27), as judged by Western blot analysis and mass spectrometry. However, the levels of Hsp27 and Hsp72 are significantly less than HAEC treated with controls (gold nanoparticles). We further demonstrate that cell death pathways are subsequently activated in nanomaterials treated HAEC, but not controls (gold nanoparticles). Gain of function experiments in which HAEC were made to over express Hsp27 and Hsp72 completely abrogated cell death pathways and resulted in the complete protection of HAEC from toxic effects of nanomaterials. Animal studies revealed that mice fed a diet containing plants known to stimulate high Hsp27 and Hsp72 blood levels were significantly protected from lung damage and infiltration of leukocytes into the lungs.      

 
Environmental Pollution and Pregnancy   
  Prof. Amal E. Mahfouz   
  Professor of Obestetrics & Gynecology, Tanta University    
  amaal_70@yahoo.com   
 
Growing evidence of the adverse effect of air pollution on human health raises the question as to what extent this affects the fetus and newborn, which are likely to be more vulnerable to environmental toxicants. Recent epidemiological studies, have reported relationship between elevated levels of air pollutants and birth outcomes. There is now emerging evidence that air pollution is associated with elevated risk of adverse pregnancy outcomes. The largest study ever conducted on air pollution's impact on newborn health has found that pregnant women exposed to black soot from urban vehicles and coal-fired power plants are more likely to have low birth-weight babies. Maternal air pollution exposure is inversely associated with fetal growth during the second and third trimester and with weight at birth and positively associated with preterm birth and SGA. Certain environmental factors are potentially harmful to a fetus, especially when the exposure is for a longer duration or of more intense nature. Environmental toxins have contributed to recurrent pregnancy loss. Caffeine, smoking, and hyperthermia are suspected teratogens. The teratogenic impact of pesticides remains unknown.      

 
Genital Anomalies and Environmental Hazards   
  Prof Dr Sherif Mohamed Shehata, MCh, CST, MD (Surg), PhD   
  Professor of Pediatric Surgery, Vice-Dean of Post Graduate Studies and Research, Tanta University, Egypt    
  sherifshehata2001@yahoo.com   
 
Toxicological effects of some chemicals on organogenesis in human fetal life are reported since 40 years. They were presented as case reports. Recently there is more awareness about the hazardous effects on pregnant women. One of the paramount effects is on genital system as reflected by threefold increase in hypospadias incidence and 2 fold increase in undecided testes recently as compared to incidence 3 decades ago. Animal proofs as described in many experiments confirmed this fact. This is documented by human prevalence of these specific genital anomalies in agricultural areas in farms of California and central Eastern Europe like Hungary in many population based studies. Occupational and environmental exposures to Endocrine Disruptor Compounds in non genetic isolated hypospadias proved in many studies. Organocholrine pesticides have been documents the deleterious effect on pregnant farm female workers. Do we have an awareness program to our female farmers or partners as we have almost the same increase in genital anomalies are still warranted. The same pesticides are used in Egypt. Multi team approaches are needed to help our community and generations as current fetuses are future leaders of the nation.      

 
   

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