ATTACHMENT F Table 2. Case SOURCE: "Aldicarb Food Poisonings in California 1985-88: Toxicity Group ASO (ppm) Age Sex Outbreak 1, Watermelon (1985): ATTACHMENT G April 20, 1990 Ms. Linda J. Fisher Assistant Administrator Environmental Protection Agency 401 M Street, S.W. Washington, D.C. Dear Ms. Fisher: .20460 On April 9, 1990 the EPA issued a joint statement with the Rhone-Poulenc Agricultural Company regarding residues of the insecticide aldicarb (Temik) in potatoes. The Committee on Environmental Hazards of the American Academy of Pediatrics is concerned that the information in the press release may mislead parents. The press release recommends that consumers "continue their normal consumption of potatoes". It is the belief of our committee that when an individual food product is found to be contaminated with a pesticide residue at a level adequate to cause illness, it is appropriate to identify the source of that hazardous product So that the public can make informed decisions about its consumption. This is particularly true in the case of parental decisions about the safety of children's food. The press release should have included a statement about aldicarb levels found in potatoes, which the committe has subsequently learned to be as high as 9.4 ppm. The committee is concerned that, if, for example, a 20 kg child were to eat a 200 gram baked potato with 9.4 ppm aldicarb sulfoxide (LD50 0.9 mg/kg), that child would receive a dose of 94 micrograms per kg of body weight. This is a level many times the threshold level for aldicarb toxicity, which was determined in the 1985 aldicarb-in-watermelon episode in California. In that epidemic the threshold of toxicity was discovered to be about 10 micrograms per kg of body weight. This is the level that the National Academy of Sciences judged to be the NOEL for cholinesterase inhibition, of which the EPA Scientific Advisory Committee has been informed. The committee is very concerned that the dose to the child consuming such a potato is only 10-fold less than the LD501 In the California outbreak, exposures to similar levels were associated with the death of a fetus of one woman, with severe hypotension and bradycardia in another woman on digoxin therapy, and with other acute illnesses in many other persons. The committee is also disturbed by EPA-Rhone Poulenc's description of symptoms likely to result from such an ingestion. The symptoms of significant aldicarb ingestion include profuse diarrhea, muscle fasciculations, bradycardia, and other cholinesterase inhibitor symptoms. These are not symptoms of "flu" despite EPA's assertion. "Flu" correctly would be associated with fever, respiratory symptoms, and muscle aches. The press release's omissions are significant. There is no identification of geographical areas where the contaminated potatoes were detected, no data on the efficacy or safety of boiling or blending of potatoes, and no interpretive insight into the press release's assertion that use of aldicarb on potatoes had not resulted in illness reports. No illness has yet been reported due to potato consumption precisely because potatoes are eaten with other foods, because clinicians would not normally be aware of a carbamate-in-food risk, and because there is poor post-market surveillance of the effects of pesticides in food. The press release should also have included a recommendation that persons who think that they may have been made ill, consult their physician who should notify appropriate public health authorities. The committee also wishes to request further information on another potentially serious recent contamination by Aldicarb, in this case involving bananas. Bananas are, of course, a major food source for young children, being consumed by 21% of all children under age six and 31% of infants on a given day. The committee wishes to commend EPA for requiring that Rhone-Poulenc carry out individual food sampling (because Aldicarb is an acute toxicant) and the committee urges EPA to provide more complete information to the public and to seek assistance from public health and child health professionals in the preparation of such reports. Members of the Academy once again offer to EPA any assistance in your agency's dealings with environmental issues that may impact children's health. Chairman MILLER. Thank you. Dr. Bearer? STATEMENT OF CYNTHIA F. BEARER, M.D., PH.D., DIRECTOR, DIVISION OF PEDIATRIC ENVIRONMENTAL HEALTH, AT CHILDREN'S HOSPITAL IN OAKLAND RESEARCH INSTITUTE, OAKLAND, CA Dr. BEARER. Yes. I would like to thank you for coming here today. The very fact that you are here shows your commitment to the health of children and their families. This is an important first step in educating the public about the environmental hazards and the special risk that they pose to children. Let me identify myself. I am Cynthia Bearer. I am a practicing doctor, and a scientist. I am Board Certified in both pediatrics and perinatal, neonatal medicine. In addition, I have a Ph.D. in biochemistry. I am an active member of Easy Bay Neonatology, and I attend here in the Neonatal Intensive Care Unit at Children's Hospital, Oakland. I am also the Director of the Division of Pediatric Environmental Health at Children's Hospital, Oakland Research Institute, and I am proud to say that this is the first such division in the country. My current research, my current interests are on how environmental exposures affect the developing fetus. And in particular, my research is dealing with both alcohol and cigarette smoking on the development of the fetus. The point I want to make here this morning, as has already been mentioned by several other people, is that children may be unwittingly serving as the canaries for our society, in terms of being the first to manifest adverse responses to environmental exposures. Why is this true? Let me explain. For two reasons. Adults and children living in the same house may experience very different environments within that house. And that a given environment may be more hazardous to the child than to the adult. Let me illustrate this with two points, using environmental tobacco smoke as an example. I think this is a timely and relevant example. As you know, (it came out in today's paper) a study is to be published in the New England Journal of Medicine on how children who are exposed to parental smoking are at two-fold greater risk that other individuals for developing lung cancer. Well, other toxic effects of environmental tobacco smoke are well-known, and I will not spend the time to describe them here. What is less well-known is that, because of the two points I am going to talk about, parents who smoke may do more harm to their children than to themselves. Let me elaborate. First, although children may be in the same macro-environment as adults, such as the house, they are actually in very different micro-environments within that house. For example, babies and infants spend a lot of time crawling or playing on the floor. It is known that heavier gases and particles, like those in environmental tobacco smoke, tend to layer out near the floor. Therefore, infants and babies are exposed to higher concentrations of these toxic chemicals. Other examples of this are radon and the volatile organic chemicals that are coming off of synthetic carpeting, which also accumulate near the floor. Secondly, a given environment may be more hazardous for the child than to the adult, for two reasons. First, the growing child has a higher metabolic rate, and therefore uses more oxygen per body weight than an adult, and therefore inhales more air per given body weight. Thus, their dose of the air pollutants will be greater. It is also known that the smoke given off the burning end of the cigarette (that is the environmental tobacco smoke) has more toxic compounds in it than the smoke inhaled by the smoker. This is true for both the respiratory irritants in the smoke, and also the carcinogenic compounds that are in the smoke. Therefore, a child in the same room as a smoking adult is receiving a higher dose of these toxic chemicals. Second, a cell is most susceptible to injury when it is growing by dividing or differentiating. And children's cells are always growing. For example, in a two-month-old child, the lung is still developing the air sacs, the alveoli in the lung. And this appears to be the reason why infants exposed to environmental tobacco smoke get sicker from common respiratory viruses and asthma, and will have smaller lung capacities. This means that all environmental hazards are more hazardous to children because their cells are more sensitive. There is little we can do to prevent toxic effects once the exposure has occurred. The cornerstone of pediatric environmental health is identification of hazards, and prevention of exposure. There are several areas in which Congress can help. What is needed is more education, for both adults and for children, on what is harmful, and how these can be avoided. We also need more research to identify both what is harmful, and who is at risk. And once a source of harmful exposure has been identified, we need the laws and means to remove it. Thank you. Prepared statement of Cynthia F. Bearer follows:] |