Exposure to environmental

It is known that the brain is one of the most sensitive sites of action of steroids in utero, and recently there have been suggestions that EDs may affect normal brain development and behaviour. For example, it has been alleged that in utero exposure to polychlorinated biphenyl compounds (PCBs) resulted in adverse effects on neurologic and intellectual function (memory and attention) in young children born to women who had eaten PCB contaminated fish in the USA." It has also been speculated that exposure to environmental pollutants with steroidal activity may be infinencing human sexual development and sexually controlled behavioiir." ... 

Human exposure to environmental contaminants has been investigated through the analysis of adipose tissue, breast milk, blood and the monitoring of faecal and urinary excretion levels. However, while levels of persistent contaminants in human milk, for example, are extensively monitored, very little is known about foetal exposure to xenobiotics because the concentrations of persistent compounds in blood and trans-placental transmission are less well studied. Also, more information is needed in general about the behaviour of endocrine disruptive compounds (and their metabolites) in vivo, for example the way they bind to blood plasma proteins. 

Immunologic Toxicity—The occurrence of adverse effects on the immune system that may result from exposure to environmental agents such as chemicals. 

Considering evidence from both field and mesocosm studies, it may be concluded that certain groups of aquatic macroinvertebrates are sensitive to pyrethroids and that there can be changes, in the short term, at the population level and above with exposure to environmentally realistic concentrations of them. It should be possible to pick up effects of this kind in natural waters using ecological profiling, for example, the River Invertebrate Prediction and Classification System (RIVPACS). There is... 

Nash, J.P., Kime, D.E., and van der Ven, L.T.M. et al. (2004). Long term exposures to environmental concentrations of the pharmaceutical ethynylestradiol causes reproductive failure in fish. Environmental Health Perspectives 112, 1725-1733. 

In some animals, consumption of a phytoestrogen-rich diet can cause temporary infertility and reproductive system disorders (Irvine, 1999). In humans, lower testosterone levels and a decline in human semen quality over the past century have been luiked to increased exposure to environmental endocrine disrupters (EDCs) (Sharpe and Skakkebaek, 1993). Furthermore, cases of sexual impotence have been reported in males exposed to synthetic estrogens in the pharmaceutical industry (Mattison et al., 1990). If this might be the case, the fetal-prepubertal period and Sertoli cell development would be of critical importance (Sharpe and Skakkebaek, 1993). However, an adverse effect of phytoestrogens on male fertility has yet to be proven. Recent work (Mitchell et al., 2001) addressing this point led to the conclusion that up to 40 mg/day of isoflavones over a two-month period had no effects on gonadotrophin and... 

Reduction of Human Exposure to Environmental iV-Nitroso Compounds... 

The complex pattern of human exposure to environmental N-nitroso compounds is summarized. Recent results are given in three areas, where a significant reduction of human exposure has been achieved after elucidation of its causes 1, N-Nitrosodimethylamine in beer. 2, Volatile N-nitrosamines in baby nipples and pacifiers and 3. occupational exposure in the rubber industry. 

Even though exposure to environmental agents such as agricultural chemicals, pesticides, and radiation has been associated with leukemia, none of these agents is linked conclusively with the development of leukemia. An increased frequency of ALL is associated with higher socioeconomic status. It is postulated that less social contact in early infancy and thus a late exposure to some common infectious agents may have some impact.7 In most individual instances, there is no reasonable or obvious explanation for the development of leukemia. 

Risk factors for the development of AML include exposure to environmental toxins, Hispanic ethnicity, and genetics.6 Of greater concern is the increased prevalence of AML as a secondary malignancy, resulting from chemotherapy and radiation treatment for other cancers. Alkylating agents, such as ifosfamide and cyclophosphamide, and topoisomerase inhibitors, such as etoposide, are linked to an increased risk of myelodysplastic syndrome (MDS) and AML.8... 

TabacovaA. 1986. Maternal exposure to environmental chemicals. Neurotoxicol 7 421-440... 

Kamel F National Institute of Environmental Health Sciences The development of neurodegenerative disease after exposure to environmental neurotoxins National Institute of Environmental Health Sciences... 

Todd AC Mt. Sinai School of Medicine, New York, NY Relationship between relatively National Institute of low-level environmental exposure to Environmental Health lead in adults and chronic neurotoxicity Sciences ... 

Woolley DE University of California, Davis, CA To determine immediate and long-term effects of exposure to environmental toxicants, especially insecticides and heavy metals (rat) U. S. Department of Agriculture... 

Baghurst PA, McMichael AJ, Tong S, et al. 1995. Exposure to environmental lead and visual-motor integration at age 7 years The Port Pirie cohort study. Epidemiology 6(2) 104-109. 

Braithwaite RA. 1987. A survey of childhood exposure to environmental lead in Walsall The importance of accuracy control. In National Meeting of the Association of Clinical Biochemists, Eastbourne, England, UK, May 11-15, 1987 Ann Clin Biochem 24 Sl-90-Sl-91. 

Fergusson DM, Fergusson JE. Horwood LJ, et al. 1988a. A longitudinal study of dentine lead levels, intelligence, school performance and behavior. Part I. Dentine lead levels and exposure to environmental risk factors. J Child Psychol Psychiatry 29 781-792. 

Tong S, Baghurst P, McMichael A, et al. 1996. Lifetime exposure to environmental lead and children s intelligence at 11-13 years the Port Pirie cohort study. BMJ 312(7046) 1569-1575. 

Centers for Disease Control and Prevention (2001). National Report on Human Exposure to Environmental Chemicals. Atlanta, Georgia. 

Calabrese, E.J., J.A. Garreffi, and E.J. Stanek. 1992. The effects of joint exposures to environmental oxidants on methemoglobin formation copper/nitrate and copper/chlorite. Jour. Environ. Sci. Health 27A 629-642. 

The most common etiology is exposure to environmental tobacco smoke, but other chronic inhalational exposures can also lead to COPD. Inhalation of noxious particles and gases stimulates the activation of neutrophils, macrophages, and CD8+ lymphocytes, which release a variety of chemical mediators, including tumor necrosis factor-a, interleukin-8, and leukotriene B4. These inflammatory cells and mediators lead to widespread destructive changes in the airways, pulmonary vasculature, and lung parenchyma. 

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