Analysis of the report entitled "The Potential Health Effects of Oxygenates Added to Gasoline" by the Health Effects Institute of Cambridge, Massachusetts in February 1996 Analysis by Peter M. Joseph, Ph.D. Professor of Radiologic Physics in Radiology University of Pennsylvania Philadelphia, PA March 10, 1996 The report prepared by the Health Effects Institute (HEI) is intended to be an extensive and definitive evaluation of the effects on public health from using oxygenates in gasoline. Such oxygenates are required in certain regions by the Clean Air Act amendments of 1990. However, in many regions where the chemical methyl tertiary butyl ether (MTBE) has been used there have been complaints from some people that they have suffered adverse health effects. In some cases, the effects reported have been severe enough to drastically reduce the quality of life of the individuals. In response to this, the CDC has conducted two epidemiologic studies that support the claim that negative health affects exist. However, other studies do not support that view. The Health Effects Institute (HEI) report attempted to review these published reports and by analysis draw an overall conclusion. Their conclusion states "Adding oxygenates to fuel is unlikely to substantially increase the health risks associated with fuel used in motor vehicles; hence, the potential health risks of oxygenates are not sufficient to warrant an immediate reduction in oxygenate use". I believe this report is seriously flawed, and that the optimistic conclusion is not only unwarranted but will encourage further expansion of oxygenate use and further increase the number of people whose health and quality of life has been diminished. The major problem stems primarily from a certain set of assumptions that they made in the analysis. There is no scientific data at present to support those assumptions, and there is considerable anecdotal evidence that they are false. These assumptions led them to reject those studies that indicate adverse health effects from MTBE and to accept those that do not. The assumptions which I believe are false are the following: 1. They assume that when MTBE is added to gasoline, all health effects are due to MTBE itself rather than to any derivative chemical produced from it. There are two such chemicals of great concern: tertiary butyl alcohol (TBA) and tertiary butyl formate (TBF). I am most concerned that TBF has been totally overlooked as a probable cause of many, but not all, of the reported symptoms. While there is no peer reviewed toxicologic data on TBF, a safety sheet published by its manufacturer says "inhalation can be fatal" and strongly suggests that it is a potent respiratory irritant. Many of the symptoms reported are typical of those produced by such irritants. The fact that most laboratory studies of MTBE do not show a strong irritant response is thus irrelevant. It is also possible that other byproducts are produced as a result of chemical interactions between the MTBE and other components of gasoline. These could explain certain symptoms, not attributable to TBF or TBA, that some people are experiencing. 2. They assume that exhaust products from engines burning MTBE gasoline are not a problem; in particular, they assume that no significant quantities of TBF are produced in the exhaust. It is true that none of the published studies of engine exhaust list TBF as a component, but that is simply because they did not choose to identify it as a specific component but lumped it together with a larger number of "volatile organic compounds" (VOC). Because TBF is an obvious oxidation product of MTBE, it is definitely expected to be produced whenever partial oxidation of the fuel takes place. Certainly, the internal combustion engine creates such a partial oxidation condition; if that were not true then only carbon dioxide and water would be produced! To assume that no TBF is produced in automobile exhaust violates the most obvious principles of elementary chemistry. One lay person1 who suffers terribly from MTBE gasoline has suggested a brilliant analogy to this problem. Suppose that in studying the health effects of smoking cigarettes scientists had not studied effects from the smoke, but had limited themselves to exposing test subjects to brief periods of smelling raw, unburned, tobacco. Of course, most people would find the odor of tobacco itself rather pleasant and certainly very few would complain of being made sick. The absurdity of such an approach is now clear since the dangers of tobacco smoke are becoming better known. There is another obvious difference; before the dangers of tobacco smoke were known, a person could choose to avoid it in most situations. In the current situation, we are being forced to breath the combustion products of MTBE continuously while being told they are actually good for our health! (Ms. Stevenson was shocked when I told her that there have been no studies of any kind on the toxicity of the actual engine exhaust gases from MTBE gasoline.) 3. They assume that ambient TBF concentrations will be less than MTBE concentrations. It is argued that ambient MTBE levels are known to be very low, on the order of 1 part per billion (ppb) except in the vicinity of gas stations. Since atmospheric chemistry2 is known to convert MTBE into TBF with an efficiency of approximately 60-70%, some conclude that TBF levels must be less than those of MTBE. That argument is not correct. The concentration of TBF in any region depends on the balance between the rate of conversion of MTBE into TBF and the subsequent conversion of TBF into other chemicals. Laboratory experiments indicate that free radicals, such as the hydroxyl radical, can easily catalyze the conversion of MTBE to TBF but are relatively inefficient in destroying TBF. Rather, one expects that ultraviolet (UV) photons from the sun will effectively photolyze the tertiary butyl moiety and produce other products. There has been no published study of the details of this reaction. However, the implications are clear. In the absence of ultraviolet photons, much of the TBF produced will accumulate. This means that even if atmospheric reactions of evaporated MTBE were the only source of TBF, the TBF levels would be expected to rise above those of MTBE at night and on cloudy days when UV photons are less plentiful. This is extremely important because many people report that their symptoms get worse at night and on cloudy days. Furthermore, this would explain why symptoms were so prominent in Alaska in the winter when daylight hours are so very short. This argument was stated in my letter3 to Archives of Environmental Health in September 1995 which was ignored by the HEI committee. Of course, when direct production of TBF from automobile exhaust is included, there is absolutely no reason to assume that ambient TBF concentrations will remain in the ppb range. Only actual measurements of ambient TBF will settle this question. 4. They assume that people with pre-existing multiple chemical sensitivity (MCS) are more likely to experience reactions to the use of oxygenated gasoline than are other people. This is a reasonable assumption, but it appears not to be true. It is definitely not true that all people who complain of problems from oxyfuel have MCS. To the contrary, the vast majority of people complaining do not experience any unusual sensitivity to other chemicals normally encountered in today's society. Perhaps more surprising, by no means all MCS victims report any unusual problems with oxyfuel. They live with a syndrome in which so many chemicals affect them that many do not report any exceptional increase in their symptom rate when MTBE is mandated in gasoline. Thus, it appears that sensitivity to the specific chemical TBF may be a condition which differs from the kind of sensitivity to an extremely broad range of chemicals seen in MCS victims. The symptoms felt by MCS victims prior to oxygenated gasoline were almost purely mental, whereas many symptoms that people experience from oxygenated gasoline are obviously physical (eye irritation, nose bleeds, sore throat, cough, etc.) The fact that some physicians believe that MCS is a purely psychiatric condition reinforces the conclusion that MCS and TBF sensitivity are different. This implies that the study that looked for MTBE related symptoms in MCS victims is certainly not definitive, nor even especially useful. 5. They assume that irritation symptoms are a "short term effect". They mean to draw a distinction from cancer and birth defects, which are observed after a period of years of exposure. However, sensitivity to irritant chemicals is known to evolve over a period of years of exposure. For example, asthma induced from industrial exposure to the chemical toluene di-isocyanate (TDI) appears in some cases after several years of exposure4. More accurately, one can say that the number of sensitized individuals increases statistically with increasing length of exposure history. This is important because some epidemiologic studies, especially the one in Milwaukee, were done after only two months of exposure. The dramatic increase in symptoms reported almost immediately in Alaska is probably due to the extremely high concentrations of TBF experienced due to the extreme winter conditions there at that time. 6. They totally neglected to even consider the possible toxic effects of TBF. However, other MTBE proponents have argued that analogous formates, such as ethyl formate, are not very toxic. That judgement is base on the relatively low oral toxicity of formates. However, it is emphatically not true that a substance of low oral toxicity can be inhaled without consequences. The most obvious common example is pepper; would the government choose to force everyone to breath pepper dust 24 hours per day forever? Furthermore, I suggest that the extreme hydrophobicity of TBF would cause it, unlike ethyl formate, to concentrate in the membranes of various cells and initiate various toxic effects. There are certainly other poisons that act primarily at the cellular membrane level. 7. Amazingly, the HEI report refused to even consider the possibility that TBF from MTBE may be increasing asthma in cities. This is despite detailed documentation that I sent them as well as my raising that point in my September 1995 letter to Archives of Environmental Health. Obviously, as a respiratory irritant TBF has to be considered at least a possible contributor to the increase in urban asthma since 1979, the year that MTBE was approved for use in gasoline. The Philadelphia Health Department is reporting an extremely high and rapid increase in asthma prevalence in children over the last few years, the time period roughly corresponding to when high (15%) levels of MTBE were required in all Philadelphia gasoline. It seems that many asthma epidemiologists think that this increase is attributable to sub-micron particulates in the air. This view is contradicted by data from the Philadelphia Department of Health which indicates that particulates, as well as all other monitored air pollutants, have been decreasing, not increasing, over this period of time. It is illogical to think that previous studies of the influence of particulates on asthma prove that TBF is not a factor when those studies were totally ignorant of even the existence of TBF. 8. Dr. Daniel Greenbaum, chairman of the HEI oxygenates committee, told me in a brief telephone conversation that TBF could not be the cause of asthma increase because it is limited to minority people in the inner city. When I stated that was not true, that suburban middle class white people were also experiencing increased asthma (although not as much as inner city minorities), he terminated the conversation. There has been absolutely no epidemiologic study of asthma problems among white suburbanites since 1992 in those regions where oxygenated gasoline was required (such as the five county Philadelphia region in Pennsylvania) that shows no increase in asthma incidence or prevalence. To the contrary, there is considerable anecdotal evidence that the opposite is true, evidence easily obtained by interviewing school nurses and athletic coaches. 9. A common assumption of several epidemiologic studies is that respiratory infections would not be affected by the use of MTBE in gasoline. That is, if a person reported any of the typical MTBE symptoms and also had an infection then the infection would be assumed to be the sole cause of the symptoms. A very real possibility is that when exposed to the respiratory irritant TBF people will experience longer and more severe respiratory infections. Again, I have anecdotal evidence supporting that view, which is entirely consistent with the known effects of such irritants. This interpretation casts doubt on the negative interpretation of the Milwaukee study. 10. All previous studies ignored the possible influence of sunlight on symptoms attributable to TBF. This is understandable because the role of TBF and sunlight was not even suspected when those studies were done. However, the HEI report does not even acknowledge the possibility that this effect may be real and does not include it in their proposals for future research. 11. Despite the fact that virtually all direct toxicologic studies of MTBE indicate only minimal toxicity, many garage and gasoline workers I know are suffering from severe illness they attribute to it. Apparently no one has considered the possibility that some of this illness could be due to an MTBE related contaminant in the gasoline. The most obvious candidate would be TBF, since it is hard to believe that commercially manufactured MTBE is 100% free of TBF. Critique of Specific Points in the HEI Report In the chapter entitled "Short Term Effects": The pages from 43 to 46 are irrelevant because they deal with animal studies of the toxicity of MTBE itself, and there are no studies of TBF in existence. page 46, "Informal Studies" quotes results obtained from the Colorado Department of Health that the number of complaints concerning oxygenated gasoline dropped from 28 the first winter (1987-88) to only 5 in 1994-95. I have spoken to several individuals living in Colorado who say they have experienced severe reactions they attribute to the use of MTBE in gasoline from the first winter. In many cases it took several winters of exposure before the people either developed the sensitivity syndrome or diagnosed its cause. All of these people are emphatic that their complaints to the Colorado Department of Health (CDH) were dismissed and ridiculed as scientifically impossible. Obviously, they quickly learned that complaining was useless; this explains the decrease in complaints that the CDH reports. I have in my possession as set of 65 symptom complaint sheets obtained in one Colorado town (Colorado Springs) during the winter of 1992-93. The symptoms reported are virtually identical to what was found by the CD in Alaska. Keep in mind that the vast majority of citizens who suffer from these effects do not realize they are due to a chemical in gasoline. They are especially unlikely to draw that conclusion when faced with claims from advertisements that oxygenates are "cleaning the air". It should be noted that the CDH has made itself a national champion of oxygenated gasoline and so will lose considerable face when it is shown to be harmful. I would not like to see national policy based on such a biased source of information. On page 47, it dismiss reports of complaints from Missoula, MT, during the winter of 1992-93 and suggests that the complaints were due to mass hysteria. This contradicts one important result quoted in the Connecticut Department of Health review 5,6 which, on page 28, says "Sixty-seven percent (12/18) of the offices contacted reported that they had received complaints from patients... there was also reported an exacerbation of symptoms among people with asthma" [emphasis added]. This is extremely important because it is the first case of a public health agency reporting an increase in asthma problems in a region recently exposed to oxygenated fuel. The HEI report fails to say that the local officials succeeded in changing the oxygenate from MTBE to ethanol the next year and that no similar complaints have been encountered since then. This is significant because both MTBE and ethanol would be perceived as "government intervention" by those citizens inclined to view oxygenated gasoline that way, so that if a mass hysteria effect were present it would be expected to show up when ethanol was mandated in gasoline in 1993-94. The fact that the HEI neglected to include these facts in its report suggests a bias against finding facts indicative of adverse health effects from MTBE in gasoline. Note that Missoula, MT, is like Fairbanks Alaska in that it is located in a deep mountain valley. This condition makes all air quality problems generated by emissions from machinery more severe than in more open environments. This may also explain why that particular community complained so vigorously about effects from oxygenated gasoline. page 47 quotes the original CDC Alaska judgement that certain symptoms, including fatigue, skin irritation, and difficulty breathing are unlikely to be due to MTBE gasoline. I strongly disagree, since I know of many people who do associate these symptoms with oxygenated fuel. In particular, several gas station workers strongly associate these symptoms with their working with gasoline. Other people found that these symptoms disappeared on travel to geographic regions where MTBE is not mandated, only to return when they returned home. Keep in mind that these are sensitivity symptoms, so it is not unexpected that different people will experience different symptoms. Certainly "difficulty breathing" is a classic symptom of someone exposed to a respiratory irritant to which he has become sensitized! page 49, the discussion of the CDC Stamford study is incomplete. They say that similar symptom rates were found in Stamford as in Albany, NY, where oxygenated gasoline was not used. What they did not say was that whereas the Stamford interviews were conducted in early April, before the major allergy season, the Albany interviews were conducted in mid May, at the peak of the allergy season. Furthermore, the CDC workers had no reason to suspect that TBF was a factor and did not pay attention to lack of sunshine as a causative factor in Stamford. The best conclusion derivable from this study is that oxygenated gasoline in April makes similar symptoms as pollen allergy in May. This is not surprising since many of the symptoms of respiratory irritants are similar to those of pollen allergy. I want to add that during 1995 many Philadelphia physicians concluded that pollen levels were exceptionally high in that city at that time. They believe that because they were seeing an unusual number of patients with allergy-type symptoms. There are two problems with that theory. First, it is not true that pollen levels were uniformly high during 1995; in fact, some physicians found that symptom rate increased after the pollen season ended in September. The second problem is that antihistamine medication was usually found to be ineffective in controlling the symptoms, indicating a problem other than conventional pollen allergies. page 49, the HEI report quotes with approval conclusions in the study by Mohr et al 7 of New Jersey garage workers indicating no unusual health effects from MTBE. I have already published a critique of that study that was ignored by the HEI. As the last sentence in that paper states, the study definitely can not rule out a sensitive subpopulation. This is obvious from the small size (11 workers) of the groups in which no differences were found. What was ignored was a slightly larger group of 13 workers in which a statistically significant difference in symptoms rates was seen, especially in the symptom rate reported on arrival at work at the beginning of the shift. This is consistent with my point that it is not only exposure to MTBE in the workplace that is causing symptoms, but to atmospheric byproducts (such as TBF) in the ambient community air. This point was ignored by Mohr et al. The reason given for ignoring the pair of groups with 13 workers was that the northern group was significantly older and slightly better educated than the second. The age difference could obviously explain any increase in non MTBE related symptoms, but it could also indicate an increased likelihood for older people to develop sensitivity to TBF. An unpublished survey of almost 800 people suffering from MTBE related illness by Dr. Myron Mehlman of Princeton New Jersey provides statistical support for that possibility. Finally, I point out that the New Jersey study was done after only 6 months of exposure to oxygenated gasoline, which is probably not enough time for the long term sensitization effects to develop. I know personally of several New Jersey garage workers who have developed very severe illness apparently associated with exposure to the gasoline. As I indicated above, some of this illness may be caused by TBF contaminating the gasoline rather than MTBE itself. It is noteworthy that the same group of New Jersey scientists who conducted that survey are far from convinced that MTBE is without adverse health effects. They are trying to organize a systematic study of controlled exposure of sensitive individuals, but the funding that they had expected from the ARCO Chemical Company has been withdrawn. pages 49-51 discuss the Wisconsin RFG telephone survey. The raw data indicate that 23% of the people felt they were experiencing "unusual symptoms" from RFG. The authors concluded that was mass hysteria due to widespread publicity. The main argument supporting that conclusion was a low rate of "unusual symptoms" reported in Chicago, with a similar exposure history but without widespread publicity. In view of the extremely short exposure time to RFG in both cities (about 2-3 months) I would not have expected the sensitive group to amount to more than 1 or 2 % of the population. Furthermore, the meaning of "unusual symptoms" could easily differ between Chicago and Milwaukee. The study found that most people complaining also had the flu. This is entirely consistent with my belief that exacerbation of respiratory infections will be shown to be a consequence of exposure to TBF. The study concluded that there were no effects that could not be explained as flu symptoms. Thus the result is anomalous and may be partly due to mass hysteria. However, because of the short exposure period it may not be a good basis on which to conclude that long term effects, such as respiratory sensitization, do not exist. Rudo has described other reasons for doubting the validity of the Wisconsin study.8 The report says (page 51) "the strongest predictors were age, having allergies, and having a cold or flu. Exposure to RFG, determined by self-reported information on the type of gasoline purchased, was not a predictor of symptoms." This is extremely important because it is entirely consistent with the TBF syndrome that I believe exists. If ambient TBF is the important factor, then the brand of gasoline, containing MTBE or some other oxygenate, is unlikely to be an important factor. Furthermore, I believe that one's sensitivity to TBF increases under conditions of epithelial inflammation, which obviously is exactly the major consequence of both allergy and respiratory infection. The association with age supports my interpretation of the New Jersey garage workers study. I could not have hoped for a sentence that would more strongly support my position! pages 51-52: "Summary of Community Studies" These pages attempt to summarize the conclusions to be drawn from the various community studies. It is remarkable how much of what they say is agreeable to me. For example: "the Wisconsin study emphasized symptom patterns considered to be 'unusual' by the respondents, an approach that may have led participants not to report increases in common symptoms that often occur chronically such as headache or eye irritation... They [the studies] do provide an imperative for further research...Also to be considered is that MTBE exacerbates the effects of other health factors. Individuals with preexisting respiratory health conditions or allergies and older people are among the groups who may be more sensitive...these studies provide an indication that some individuals exposed to emissions from automotive gasoline containing MTBE may experience acute symptoms such as headache or eye and nose irritation." What is amazing is that in view of these facts, the HEI committee nevertheless concludes that [front page] "the potential health risks of oxygenates are not sufficient to warrant an immediate reduction in oxygenate use". Unless there is some overwhelming advantage to public health from the use of oxygenates, it is difficult to see how this conclusion can be derived from all of the preceding data and uncertainties. ARE THERE ADVANTAGES TO MTBE? The two major advantages claimed for oxygenates in gasoline are reduction of carbon monoxide and ozone. I believe both of these are quantitatively very minor, controversial, and medically irrelevant. The reduction of carbon monoxide is claimed to be about 13-20% for gasoline with 15% MTBE. This is based on laboratory measurements of cars without so-called "closed loop" air/fuel control systems. Modern cars with such systems are expected to operate in such a way as to defeat the anticipated benefits of oxygenating fuel by forcing the engine to burn a richer fuel/air mixture. This may explain the substantial reduction in gas mileage reported by thousands of motorists. Presumably this issue will be addressed by another expert committee. However, several urban air quality studies known to me do not indicate any significant reduction in CO since oxyfuel was initiated. These studies have been done by Professor Larry Anderson, University of Colorado, Dr. Kenneth Rudo, State of North Carolina Health Department, and Professor Paul Lioy, New Jersey College of Medicine. page 92, the HEI report quotes studies showing a reduction of a few (roughly 5%) percent in the time to pain from a 2% saturation in hemoglobin. It is claimed that this is clinically significant. None of the physiologists or cardiologists that I have questioned agree. A 2% saturation is considered generally negligible clinically. Furthermore, if the ambient CO level reaches its current limit of 9 ppm for 8 hours, that will produce a hemoglobin saturation of about 2%. Therefore, a 10% reduction in this quantity will presumably mean at most a decrease in saturation of 0.2%. It is absurd to imagine that this will significantly increase the quality of life of any person with marginal heart function. For example, if such a person could jog for 10 minutes without angina with CO at 9 ppm, the expected reduction of CO from MTBE would increase his jogging time by only 3 seconds! It should be emphasized that in most cities CO levels only occasionally exceed 9 ppm. The reduction in ozone is claimed to be greater, perhaps as much as 30-40%. This seems to be purely hypothetical, since in all areas of the east coast where RFG was used for the first time in 1995 the ozone levels were exceptionally high, not low. Atmospheric experts blame unusual weather. However, I have data that shows that temperature alone can not explain the high ozone levels in 1995. It is expected that decreased ozone levels will help asthmatics, which is true if they are really achieved. It is ironic that the two groups of people intended to be helped by oxygenated gasoline are, in the opinion of myself and hundreds of other laymen, precisely those that are being hurt. I have explained previously my belief that asthmatics are being not only hurt by the ambient TBF from MTBE, but their numbers are rapidly growing in many areas where MTBE has been used the longest. More controversial perhaps is the hypothesis that TBF is also creating cardiac problems. The mechanism here is apparently neurological, producing chemically induced anxiety and palpitation reactions that in some individuals produce arrhythmias. I know of several anecdotal accounts of death of unexplained origin that are consistent with this picture. A recent article in the New York Post indicated that heart attacks are increasing in New York City in recent years. If MTBE is not canceled soon, a epidemiologic study of these possible problems is imperative. RESEARCH PRIORITIES On pages 103 to 105 the HEI report gives its recommendations for research priorities. This is very troubling because it totally ignores what are the two most pressing issues. Namely, is asthma getting worse or better as a result of MTBE usage, and what are the effects of exhaust gases on public health? The very extensive research on acute effects of MTBE are important for people such as gas station workers, but a much more direct method would be to simply study the health of those workers over a period of time. The neglect of exhaust gases may be predicated on the idea that catalytic convertors eliminate such toxic compounds as TBF. That grossly exaggerates the effectiveness of those devices. Even if they reduce the level of toxic emissions by, say, a factor of ten, one can not conclude that the remaining exhaust gases are benign. One approach, not recommended by the HEI committee, would be to study the relative toxicity of actual engine exhaust gases on people who complain of sensitivity, comparing the effect of adding MTBE to the fuel mixture. CONCLUSION In view of all of these uncertainties and assumptions, the question arises why the government should continue to press to expand the use of oxygenated gasoline. I maintain there is not a shred of evidence that oxygenated gasoline is actually helping anyone. In fact, all of the anecdotal evidence known to me indicates that it is most hurting people with asthma and heart disease, the very people it was intended to help! The easiest way to clarify these questions is to compare health effects in regions required to use MTBE and those not required. Coupled with actual ambient measurements of TBF, this will enable a meaningful comparison to be made. Such a comparison requires that we preserve those areas of the country, such as Vermont, and "upstate" Pennsylvania, New York, and Maine as regions of minimal MTBE usage. The contrary policy of continually expanding the use of oxygenated gasoline to all regions of the country will make such studies immeasurably harder and greatly delay, probably for many years, the time before the consequences of mass exposure to TBF are understood. During this time certainly thousands, and probably millions, of people will have their health and quality of life unnecessarily diminished. REFERENCES 1. L.C.Stevenson, "Personal Communication March 9, 1996," (PO BOx 3645, Woodbridge,CT, 1996), pp. 1-1. 2. D.F.Smith, T.E.Kleindienst, E.E.Hudgens, C.D.McIver, and J.J.Bufalini, "The photooxidation of methyl tertiary butyl ether," Int. J. Chem. Kin. 23, 907-924 (1991). 3. P.M.Joseph, "Letter: Atmospheric Byproducts of MTBE as a Source of Community-wide Illness," Arch. Env. Health 50, 395-396 (1995). 4. X.Baur, W.Marck, J.Ammon, A.B.Czuppon, B.Marczynski, M.Raulf-Heimsoth, H.Roemmelt, and G.Fruhmann, "Respiratory and other hazards of isocynates," Int. Arch. Occup. Environ. Health 66, 141-152 (1994). 5. M.L.Fleissner, H.Rao, G.Ginsberg, and D.Pelletier, "Methyl Tertiary Butyl Ether (MTBE): A review of exposures and potential health effects," (CT Dept. Public Health, Hartford,CT, 1996), pp. 1-65. 6. A.Unknown, "Oxygenated fuel data collection: Missoula Physician Screening Jan 20, 1993," (MCCHD, Missoula, MT, 1993), pp. 1-2. 7. S.N.Mohr, N.Fiedler, C.Weisel, and K.KellyMcNeil, "Health-effects of MTBE among New Jersey Garage Workers," Inhalation Tox. 6, 553-562 (1994). 8. K.Rudo, "Review of the Wisconsin DHSS Final Report Titled: An Investigation of Health Concerns Attributed to Reformulated Gasoline Use in Southeastern Wisconsin," (N.C.Dept.Env, Rayleigh,NC, 1995), pp. 1-7.