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Chemical Disease

Disease is a cellular process in which cells malfunction individually and collectively, undermining the tissues and organs they comprise. Toxic chemicals may act in a multitude of ways to attack cells and undermine their function in the body. Toxic effects are generally classified as either immediate (acute) or long term (chronic) (Chapter 5). Acute toxicity is manifested minutes to days following exposure. Examples are carbon monoxide poisoning, snake bites, and drug overdoses. Chronic toxicity is slow in onset, and months or years may pass before a harmfnl effect becomes apparent. Examples are cancer, infertility, IQ deficit, and hypertension. [Pg.119]


Schwinn, F.J., and Urech, P.A. 1981. New approaches for chemical disease control in fruit and hops. Proc. Brit. Crop Prot. Conf. Insecticides, fungicides 3, 819-833. [Pg.105]

Amphibian deformities related to chemicals, disease and radiation (Harris et ah, 1998a, b Dalton, 2002). [Pg.5]

The relational database was queried to separate out the unique terms and find out the number of times they occurred. A total of 4.3 million biomedical terms were identified and put in an internal dictionary. These terms were classified into five major groups of proteins, genes, chemicals, diseases, and organisms. The cooccurrence, in the abstracts, of each of the terms with the others was calculated. This co-occurrence is just considering the keywords, the noise words will help to understand whether the co-occurrence is positive or negative. [Pg.439]

Acute Versus Chronic Exposures Exposures can be acute or chronic. For some chemicals, a single exposure is sufficient to induce an effect. For other chemicals, disease or effects do not appear until after repeated exposures. Some materials will not cause permanent damage with a single exposure. Other materials require one exposure to cause damage. Some may not cause permanent damage at all. [Pg.341]

Guerzoni, E. and R. Marghetti. 1987. Analysis of yeast flora associated with grape sour rot and of the chemical disease markers. Appl. Environ. Microbiol. 53 571-576. [Pg.350]

There are two basic approaches to designing an epidemiological study to investigate accidentally induced chemical disease cohort and case control. In a cohort study, the at-risk population is defined as one that is known to have been exposed to a chemical of concern, and the frequency of disease is compared with that of a control population that has not been exposed. More than one disease may be tracked in a cohort study, depending on the known or suspected toxicides of the chemical of concern. Elevation of disease frequency, i.e., rejection of the null hypothesis at an acceptable level of statistical confidence, constitutes presumptive evidence of a causal link between exposure and disease. The causal connection can be strengthened by evidence of a dose-effect relationship, as discussed in Section 4.5. [Pg.60]

Describe the kinds of toxicological evidence that serve to substantiate and strengthen epidemiological (statistical) evidence of chemical disease. [Pg.64]

Rejection of the null hypothesis provides prima facie statistical evidence of increased disease incidence in an at-risk population however, it does not constitute conclusive proof. One or more of several other lines of evidence are needed to buttress the statistical finding (a) evidence that the at-risk population has been exposed to the toxic chemical (b) evidence from toxicity testing in animals or from accidental human exposures that the chemical produces the disease symptoms observed in the at-risk population (c) evidence that the molecular mechanism of action is consistent with the observed disease symptoms and/or (d) evidence that the incidence of chemical disease conforms to a dose-effect relationship. [Pg.65]

The Rate oe Increase in Chemical Disease Frequency as a Function oe Dose... [Pg.81]

While relatively rare compared with the large number of detoxication reactions performed by Phase I and II enzymes, toxication reactions pose significant risks of chemical disease. In recognition of their potential to increase the risk of cancer. [Pg.106]


See other pages where Chemical Disease is mentioned: [Pg.25]    [Pg.139]    [Pg.14]    [Pg.104]    [Pg.37]    [Pg.14]    [Pg.170]    [Pg.325]    [Pg.194]    [Pg.93]    [Pg.98]    [Pg.739]    [Pg.38]    [Pg.56]    [Pg.57]    [Pg.59]    [Pg.61]    [Pg.84]    [Pg.119]    [Pg.121]    [Pg.123]    [Pg.125]    [Pg.127]    [Pg.129]    [Pg.131]    [Pg.133]    [Pg.143]    [Pg.1]    [Pg.175]    [Pg.345]   


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