A Reply to Rothenberg
A Reply to Rothenberg
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对罗滕伯格的回复
DOI:
10.1044/jshd.4702.220
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发表时间:
1982
期刊:
影响因子:
--
通讯作者:
J. R. Smitheran
中科院分区:
文献类型:
--
作者:
T. Hixon;J. R. Smitheran
A response is necessary to a potentially misleading letter in the May, 1981 issue. Under the title," Caution.,. Peanuts May be Harmful to Your Clients' Health!",(Putnam, 1981) information concerning the inhalation toxicology of oil was brought to light by Anne HB Putnam of the University of Arizona. Her reasons for discussing the inhalation toxicology of oil, particularly the oil found in peanut products centered on a positive reinforcement mode of speech and hearing testing. This type of reinforcement in speech and hearing testing is apparently sometimes useful, and seems to be the reason that this letter found its way to JSHD. However, Putnam has accumulated enough toxicological information concerning the adverse effects from the inhalation of oils to suggest that the peanut products used in this form of testing can bepotentially harmful to the client because of their oil content. From a toxicological standpoint this suggestion is completely absurd. A rudimentary concept central to toxicology is the doseresponse curve of adverse effects. Simply, the greater the dose administered, the greater the response or adverse effect. Accordingly, any normally innocuous substance is potentially harmful if the dose is sufficient. Consider the" dose" of oil a client described by Putnam would receive from an inhaled peanut particle. This amount is far less than the virtually negligible amount one would be able to squeeze from the peanut. The reference cited by Putnam (Robbins & Cotrau) concerning the pathology of lipoid pneumonia states that" aspiration of oil is usually encountered in infants and children who are forced to swallow cod liver oil against their resistance"(p. 826). This makes it appear that an appreciable amount of oil, on the order of a teaspoonful, need be accidentally inspired to produce the adverse effect. This quantity of oil is certainly not going to be present in the lungs of a client inspiring a peanut product. Simply consider the number of peanuts eaten in this country without lipoid pneumonia being cited as a potential danger. Another fundamental question of toxicological interest raised by Putnam's letter is one of risk assessment. This process separates the" hazard"(the intrinsic toxicity of an agent) from the" risk"(the probability that a toxic dose can be received). In the case of inhaled peanuts causing lipoid pneumonia the hazard is barely existant, and hence the risk is extremely low. Logically, the hazard of asphyxiation from a solid object inspired into the lungs is high, and therefore the risk of asphyxiation from an inspired peanut is great. At the risk of sounding somewhat shrill, it seems ludicrous that a clinician can seriously worry about the potential of lipoid pneumonia developing and harming a client who has the potential to inhale a peanut, and not be concerned about asphyxiation. Happily, it appears that Putnam's fears of being sued for malpractice by a client who has developed lipoid pneumonia from peanut inhalation are groundless. This should therefore enable her to refrain from dabbling further in toxicology, and limit herself to matters related to speech and hearing.