Review of Inhalants - ARCHIVES - National Institute on Drug Abuse

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In dogs, the threshold saturations that produce cardiac changes were determined by Ehrich et al. (1944). There was depression <strong>of</strong> the R-T segment and degenerative changes for a few hours at 40% carboxyhemoglobin. Heart block and myocardial hemorrhages and necroses were observed only when the carboxyhemoglobin level exceeded 75% for 1 hour or longer. In rats poisoned with 10,000 parts per million (ppm) carbon monoxide inhalation for 10 minutes, high enough to elevate carboxyhemoglobin to 65%, ultrastructural changes in the heart, consisting <strong>of</strong> intracellular edema, swelling <strong>of</strong> mitochondria, and disruption <strong>of</strong> lysosomes, were reported. Suzuki (1969) concluded that the effects <strong>of</strong> carbon monoxide on the heart result not only from hypoxemia but also from the direct toxic effects on the specific respiratory enzymes. Twenty-four hours after the inhalation, the hearts <strong>of</strong> most rats appeared essentially normal so that the toxic effect was reversible. From the foregoing experiments, cardiac arrhythmias appear only if carboxyhemoglobinemia exceeds 40 percent, which is not attained during ordinary use <strong>of</strong> methylene chloride. Interaction Between Carboxyhemoglobin and Solvents on the Heart For completeness, it is necessary to discuss the question <strong>of</strong> interaction between the direct cardiac effects <strong>of</strong> methylene chloride and the indirect cardiac consequence <strong>of</strong> carboxyhemoglobinemia resulting from metabolism <strong>of</strong> methylene chloride. Does carboxyhemoglobinemia increase the vulnerability <strong>of</strong> the heart to epinephrine-induced arrhythmia? The answer was supplied in 1974 by Kaul et al. In dogs with elevated levels <strong>of</strong> carboxyhemoglobin (to 35%) by inhalation <strong>of</strong> carbon monoxide, there was no increase in vulnerability <strong>of</strong> the ventricles to arrhythmias provoked by epinephrine and petroleum ether. There are no experiments reported involving methylene chloride. However, it is safe to conclude that carboxyhemoglobin, per se, does not increase the sensitivity <strong>of</strong> the heart to hydrocarbon-epinephrine arrhythmias and that although methylene chloride is converted to carbon monoxide, this does not increase the vulnerability <strong>of</strong> the heart. In other words, the arrhythmogenicity <strong>of</strong> methylene chloride is not enhanced by the small amount <strong>of</strong> carbon monoxide produced by its metabolism. Myocardial Contractility It was stated earlier that the threshold concentration that would depress significantly myocardial contractility <strong>of</strong> the canine heart is 2.5% methylene chloride. Since this was performed in an intact animal, it was not possible to differentiate the effects <strong>of</strong> carbon monoxide formation separately from the nonmetabolized solvent. Experiments recently completed have succeeded in the identification <strong>of</strong> cardiac effects related and unrelated to carbon monoxide (Juhasz-Nagy et al., 1977; Zakhari et al., 1977). 169
In the canine heart-lung preparation, the inhalation <strong>of</strong> methylene chloride was not accompanied by a rise in carboxyhemoglobin. Thus, it was possible to identify the myocardial depressant action <strong>of</strong> methylene chloride alone without formation <strong>of</strong> carbon monoxide. In the dog with intact heart, the hemodynamic effects <strong>of</strong> methylene chloride alone were not exaggerated by the combined administration <strong>of</strong> carbon monoxide. This ischemic heart was no more reactive to methylene chloride and to carbon monoxide compared to the nonischemic heart. Furthermore, the initial elevation <strong>of</strong> carboxyhemoglobin following the inhalation <strong>of</strong> carbon monoxide was not influenced in its normalization pattern by the inhalation <strong>of</strong> methylene chloride. These results indicate that the metabolic conversion <strong>of</strong> methylene chloride to carbon monoxide does not occur in the heart, does not influence the normalization <strong>of</strong> carboxyhemoglobinemia even in the presence <strong>of</strong> methylene chloride, and that carboxyhemoglobinemia does not exaggerate the cardiac effects <strong>of</strong> methylene chloride. As a matter <strong>of</strong> fact, the author believes that conversion to carbon monoxide reduces the cardiac depressant action <strong>of</strong> methylene chloride in as much as the same concentration is more depressant in the heart-lung preparation where there is no formation <strong>of</strong> carbon monoxide, compared to the heart <strong>of</strong> an intact animal where metabolism is possible. Acetylene Dichloride Acetylene dichloride (CHClCHCl) is used as a solvent for waxes, resins, acetyl cellulose, and rubber. It is contained in some antiknock gasolines, fumigant mixtures, and in cleansing products. There is one reported fatality after inhalation <strong>of</strong> the acetylene dichloride vapor in a small enclosure (Hamilton, 1933). Menshick (1957) reported four others and collected 27 instances <strong>of</strong> occupational poisoning from the literature. There were pathological lesions in the liver and kidneys. Ethylene Dichloride Ethylene dichloride (CH 2ClCH 2Cl) is a constituent <strong>of</strong> rubber cement , degreasing solvent mixtures, and leaded fuels. The Criteria Document (1976b) reviews almost a hundred cases <strong>of</strong> accidental poisoning and occupational inhalation <strong>of</strong> ethylene dichloride. Hepatic and renal lesions are the major lesions seen at postmortem examination. Propylene Dichloride This solvent is a component <strong>of</strong> furniture finisher, paint remover, and soil fumigants. A case <strong>of</strong> acute poisoning from oral ingestion <strong>of</strong> propylene dichloride (CH 2ClCHClCH 2) was reported by Chiappino and Secchi (1968). Histologic studies <strong>of</strong> the liver biopsy showed diffuse phenomena <strong>of</strong> turbid degeneration <strong>of</strong> the liver cells and ultrastructural changes in Golgi apparatus, mitochondria, and 170
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Review of<
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ACKNOWLEDGMENT The Research Triangl
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PREFACE Inhaling psychotropic subst
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Perhaps society can begin to look o
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Mr. Joseph P. Nachtman Graduate Res
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CONTENTS (con.) Danger to Self and
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CONTENTS (con.) Acute Toxicity <str
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CONTENTS (con.) Chapter 11 Nervous
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CONTENTS (con.) Areas of</s
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Chapter 1 INHALANT ABUSE: AN OVERVI
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A special group of
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intoxication. Industrial workers ar
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most common complaints noted during
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SUMMARY Inhalant abuse, a youthful
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SOCIOCULTURAL-EPIDEMlOlOGlCAL ASPEC
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use of mind alteri
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2. Another reason is the nature <st
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Rates for inhalant use are on about
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with Indians, and blacks also are m
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Chambers, C., J. Inciardi, H. Siega
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Appendix SUMMARY OF EXPLORATORY STU
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New York Miami Louisville Los Angel
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Chapter 3 CLINICAL EVALUATION OF PS
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peer ratings of re
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The literature generally provides l
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MENTAL STATUS OF USERS Cognitive Di
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Tinklenberg and Woodrow (1974) cont
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Psychotic Organic Brain Syndrome (O
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Beer Marihuana Spray paint Liquor G
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Lachar and his colleagues (in press
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work setting while providing for an
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2. sniffing, unobtrusive or nonreac
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De la Garza, F., I. Mendiola, and S
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Maletzky, B. Assisted covert sensit
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MEDICAL EVALUATION OF INHALANT ABUS
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are not actively avoided. Table 1 s
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TABLE 1 SUMMARY OF CLINICAL SYNDROM
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Aerosols Abuse of
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either peripheral neuropathy or myo
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DATA SUMMARY Table 2 summarizes the
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Ear disease Nose, sinus, throat Fai
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over-the-counter drugs or use <stro
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The patient is asked to stand, to w
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Bass, M. Sudden sniffing death. JAM
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Storms, W. Chlorof
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(Taher et al., 1974), permanent adv
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during the course of</stron
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abuser, particular attention would
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Reinhardt, C., A. Azar, M. Maxfield
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NEUROLOGICAL HISTORY A. Record onse
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NEUROLOGICAL EXAMINATION (Items to
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VII. FACIAL MOTOR (VOLITIONAL, EMOT
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E. SENSORY: Chart deficits in: Pain
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Chapter 6 INTRODUCTION Daniel Couri
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TABLE 1 OCCURRENCES OF VOLATILE SUB
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Chapter 7 ABUSE OF INHALATION ANEST
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GASES Name Nitrous Oxide Ethylene C
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Generic Name Trade Nitrous Oxide No
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INCIDENCE AND CONTROL OF ANESTHETIC
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Deniker, P., M. Cottereau, H. Lôo,
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Chapter 8 TOXlCOLOGY OF ALCOHOLS, K
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The time course of
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TABLE 1 ACUTE TOXICITY OF ALCOHOLS
Page 139 and 140: Industrial exposure to ketones occu
Page 141 and 142: Despite widespread use of</
Page 143 and 144: It has been shown that methyl ethyl
Page 145 and 146: Chapter 9 TOXICOLOGY OF ALIPHATIC A
Page 147 and 148: percent of an oral
Page 149 and 150: individuality in resistancce to ben
Page 151 and 152: to intoxicate himself within 1 to 3
Page 153 and 154: Organ Toxicity Animal. Toxicity stu
Page 155 and 156: 1961). The threshold limit value fo
Page 157 and 158: imately 3 percent of</stron
Page 159 and 160: several intermediates to 1,2-dihydr
Page 161 and 162: n-Hexante n-Hexane (CH 3(CH 2) 4CH
Page 163 and 164: toxicity. Frommer et al. (1974) not
Page 165 and 166: gests that death may result in some
Page 167 and 168: incoordination, prostration, and co
Page 169 and 170: i.v. the LD 50 was 51 mg/kg Dewey e
Page 171 and 172: II. Animal and human response to va
Page 173 and 174: Elkins, H. The chemistry of
Page 175 and 176: Grant, W. Toxicology of</st
Page 177 and 178: exposure with mortality and toluene
Page 179 and 180: Nomiyama, K. Studies on poisoning b
Page 181 and 182: Reinhardt, C., A. Azar, M. Maxfield
Page 183 and 184: Tauber, J. Instant benzol death. J
Page 185 and 186: Chapter 10 PRECLINICAL PHARMACOLOGY
Page 187 and 188: TABLE 1 INHALATIONAL TOXlCITY OF FL
Page 189: There is no question that methylene
Page 193 and 194: is used as a solvent in cosmetic an
Page 195 and 196: mean aortic pressure, and mean pulm
Page 197 and 198: Pretreatment of ra
Page 199 and 200: FC 11 FC 12 Compound Carbon tetrach
Page 201 and 202: National I
Page 203 and 204: Their toxicity and potential danger
Page 205 and 206: Zakhari, S., and D. Aviado. Cardiop
Page 207 and 208: include photophobia, irritation <st
Page 209 and 210: compound or of ano
Page 211 and 212: portions of the sc
Page 213 and 214: chicken, cat, rat, and mouse. The k
Page 215 and 216: The combined solvents encountered i
Page 217 and 218: CONCLUDING REMARKS Little is known
Page 219 and 220: Saida. K, J. Mendell, and H. Weiss.
Page 221 and 222: Chapter 12 PRECLINICAL BEHAVIORAL T
Page 223 and 224: The squirrel monkey has been shown
Page 225 and 226: dependency. It may be possihle to i
Page 227 and 228: spectrum of solven
Page 229 and 230: without adverse effects. Threshold
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Page 233 and 234: ear problems (Patterson and Bartlet
Page 235 and 236: Ishikawa and Schmidt (1973) noted t
Page 237 and 238: statistically significant, it is di
Page 239 and 240: The very early age at which solvent
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Bushnell P., P. Malof</stro
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Parkhouse, J., J. Henrie, G. Duncan
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SUMMARY 225
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PREVENTION Abuse prevention is inte
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generally, to not using those subst
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drugs. Typical situations o
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to use appropriate controls or comp
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ents and neighbors in recreational
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eyond a week or two. This may be du
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not appear to be too useful as a te
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protocol for exposing an animal to
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BIBLIOGRAPHY 243
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Abdel-Rahman, M., L. Hetland, and D
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Angel, C., H. Bounds, and A. Perry.
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Anonymous. Hepatorenal damage from
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Aono, K., H. Tateishi, and D. Karas
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Azar, A., H. Trochimowicz, J. Terri
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Bateman, M. Functional taxonomy <st
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Berlin, M., J. Gage, and E. Jonnson
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Bonnevie, A. [Letter: Acid hardened
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Buday, M., M. Labant, and G. Soós.
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. Petroleum hydrocarbon toxicity st
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Clearfield, H. Hepatorenal toxicity
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Criteria Document. Criteria for a r
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Deguchi, T. Changes in serum trans
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DiVincenzo, G., F. Yanno, and B. As
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Dürr, M. Pressurized aerosols. A n
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Faure, J., H. Faure, M. Yacoub, R.
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Forni, A., A. Cappellini, E Pacific
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Gellman, V. Glue-sniffing among Win
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Gothe, C., P. Ovrum, and B. Hallen.
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Haraszti, A., and M. Sovari. Fatal
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Herbolsheimer, R., and L. Funk. [Ga
Page 308 and 309:
Huff, J. New evidence on the old pr
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. The interaction of</stron
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Kaminski, M., et al. Some histochem
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. Metabolism, excretion, and toxico
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Konyaeva, A., and F. Vishnevetskii.
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Lafontaine, A., et al. Toxicity <st
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October 24-26, 1973. Conclusions an
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Lovius, B. Letter: Aerosol adhesive
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mation by mass spectrometry. Novemb
Page 326 and 327:
Merry, J. Glue sniffing and heroin
Page 328 and 329:
Mouton, N. [28 cases of</st
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Niazi, S., and W. Chiou. Fluorocarb
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of trichloroethyle
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Patterson, M., and P. Bartlett. Hea
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Posner, H. Biohazards of</s
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Ratney, R., D. Wegman, and H. Elkin
Page 340 and 341:
Rosenberg, P. The effect of
Page 342 and 343:
Sato, Y., and M. Maruyama. Immunolo
Page 344 and 345:
Schmidt, P., I. Ulanova, G. Avilova
Page 346 and 347:
Shepard, R., and J. Rose. Alcohol.
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Sjöberg C. [Hobby activity and dea
Page 350 and 351:
Spierdijk, J., and V. Regjer. Dange
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Strusevich, E., V. Fedianina, O. Sa
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. Cardiovascular effects of
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Tinklenberg, J., and K. Woodrow. Dr
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Trochimowicz, H., A. Azar, J. Terri
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arbital sleeping and zoxazolamine p
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Waizer, P., S. Baez, and L. Orkin.
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Wijekoon, P., N. Sivaramakrishna, a
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Zimmerman, S., K. Groehler, and G.
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4 NARCOTIC ANTAGONISTS: THE SEARCH
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27 PROBLEMS OF DRUG DEPENDENCE, 197
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44 MARIJUANA EFFECTS ON THE ENDOCRI
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DHHS Publication No. (ADM) 85-533 P
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Review of Inhalants - ARCHIVES - National Institute on Drug Abuse

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