Document NEZgE8kjxdxYNz7RkzeNwM7DD

INTERNAL CORRESPONDENCE FROM R. T. Cheng TO Wilbur Shyeh subject PVC FIRE FIGHTING date June 28, 1976 Hydrogen chloride inhalation has been a serious problem for fire fighters in fighting polyvinyl chloride fires. The attached article explains the problem and recommends a few preventive measures. RTC/ELK cc: R. L. G. M. Ed Lu H. E. Gibson, Hale Runion M.D. R. T. Cheng CUSAROSS 00812 SAFETY INFORMATION C-92 From R. G. Goldthwait June 18, 1976 Polyvinyl Chloride Toxicity in Fires Hydrogen Chloride Toxicity in Fire Fighters Robert F. Dyer, MD. Victor H. Esch, MD Polyvinyl chloride, of all the plastic polymers, has been implicated pri marily in causing the most serious problem in fire fighting today because it releases hydrogen chloride gas when burning. One hundred seventy tire fighters who experienced symptoms from its toxicity have been studied from 1970 to 1975, One died. (JAMA 235:393-397, 1976) A RECENTLY identified hazard that is of paramount importance to prac ticing physicians is that of chemical injury incurred by persons exposed to fumes from fires. Specifically, such in juries are caused by the inhalation of vapors created hy the thermal degra dation of polyvinyl chloride, a plastic polymer. Such substances have now liccomc widely used in the construc- See also p 390. tion of homes, furnishings, office equipment, electric wire, telephone and cable covering, and vehicles. A particular hazard exists in the case of the fire fighter, although it could be equally serious in any circumstance in which an individual might he exposed to such plastic combustion products. THE FIRE At 10:30 am on Jan 6,1970, an alarm sounded for a fire reported to be on the sixth floor of Building 213 at the Washington, DC, Navy Yard. Units of the District of Columhia Fire De partment arriving on the scene found the floor filled with a heavy concen tration of toxic fumes. Although all of the fire fighters carried masks, none were used, since neither the fire nor From the Police and Firemens Clinic, Wash ington. DC. Reprint requests to Chairman of the Board o< Surgeons. Suite 1445. Chevy Chase Bldg. 5530 Wisconsin Ave. NW, Washington, DC 20015 (Dr Dyer). the smoke was so excessive as to pre vent entry without masks. The fire, which was confined to an office copy ing machine constructed of plastic and Teflon parts, was quickly extin guished. The fire companies entered the building via the elevator, placed sev eral portable fans for ventilation, and left the building about 20 minutes later. On returning to their quarters, many of the fire fighters experienced unusual and unexplainable symp toms, including a constricting tight ness localized to the anterior part of the chest. This chest discomfort was described as a soaring, burning sensa tion accompanied by dyspnea as well as a ''horning sensation appearing to close off the throat." These symptoms were in addition to the usual head ache, dizziness or vertigo, and nausea, which, in our experience, is fre quently seen in cases of nonchemical smoke inhalation. Some symptoms persisted over a course of several days following exposure to the fumes. The dyspnea was noted on mild exer tion and was associated with moder ate apprehension hy all of the af fected fire fighters. A number of the fire fighters exposed at this fire expe rienced severe conjunctivitis, lacrimation, and dyspnea persisting for 24 hours after the fire. An intense head ache, localized anteriorly and persist ing about 24 hours, was also common. REPORT OF A CASE Approximately 24 hours after the fire, a XT-> ear-old fire fighter fainted in the sit ting room of the truck company. It was also re|)orled that he had a muscle spasm similar to an epileptic seizure, but man ured, was fully conscious, and got up im mediately. His superior officer asked how he felt, and he replied that he was "fine" and walked into the kitchen. Following lunch, the acting sergeant on duty looked for the man to cheek his condition for driv ing and found him lying on the door next to his hcd. He was cyanotic and, despite all resuscitative efforts hy an ambulance crew t and the rescue squad, was pronounced dead on arrival hy a fire surgeon at 'he (leorgc Washington Uni\ersit\ Hospital at 1:11) cm. Postmortem examination by the District of Columbia Department of Public Health Medical Examiner showed severe pulmonary hemorrhage and edema due to chemical pneumonitis secondary to expo sure to chemical smoke and fire The pathologist also reported corona rv atherosclerosis. EFFECT OF FUMES It has been suspected for several years that the smoke and fumes front electrical fires produced greater in jury now than similar fires in the past.' - It was strongly suspected that hydrogen chloride released hy ther mal degradation of PVC, a common electrical wiring insulation material, was the lethal product causing death in this instance. The medical exam iner's report and the microscopic findings subsequently confirmed our original clinical impression of the cause of death. Hydrogen chloride, inhaled either in the gaseous state or combined with water vapor, acts as an irritant to (lie mucous membranes of the o\os and JAMA. Jan 26. 1976-Vol 235, No 4 Polyvinyl Chloride--Dyer & Esch 393 CUSAROSS 0081 V* - 800 CQL. OC Co U4coc> O - 600 _ODo o o> o -C 400 <cn 0Q c u T0oV>1, oQ. X 200 Fig 1.--Hydrogen chloride concentration and optical density of polyvinyl chloride electri cal insulation decomposition products. the respiratory tract. An HC1 concen tration of 15 ppm causes localized irritation to the throat after short ex posure. Hydrogen chloride concentra tions of 50 to 100 ppm are tolerable for one hour by humans. More severe exposures result in pulmonary edema and often in laryngeal spasm. Con centrations of 1,000 to 2,000 ppm of HC1 are dangerous even with brief exposure1 (Fig 1). Quantitative release of HC1 on thermal degradation of PVC has been well documented in the scientific and medical literature. Polyvinyl chloride, of all the synthetic plastic polymers, has been implicated as causing one of the most insidious, serious problems in fire fighting today, due to its re lease of HC1 gas while burning. Mists of hydrochloric acid are considered less harmful than anhydrous HC1 be cause the droplets have no hydrating action. Animal Experiments The toxicity of PVC has been sub stantiated by Kishitani* in his com prehensive animal experiments per formed at the University of Tokyo. With respect to the toxicity of carbon monoxide, Kishitani states that the injurious nature of PVC is unique. All mice exposed to harmful gas products died, hut the carboxyhemoglobin con centration in the dead animals was low (average, 21.2%). This clearly in dicated that the fatalities were not due directly to CO poisoning. At au topsy, the eyes of the mice were closed, their mucous membranes were injured by chemicals, and the sclerae were discolored. The latter had be come white due to the action of chlo rine gas. All of the mice died in a pe riod of 15 minutes after exposure to PVC fumes. Electrocardiographic ab normalities appeared prior to gener ation of large quantities of smoke. This indicated that a harmful gas produced at an early stage was caus ing the effect. Similar results were found on exposure to polyurethane gas. Kishitani concluded that the in jurious properties of burning mate rials such as wood, fire retardant ply wood, melamine finishing board, and acrylic resin are due to CO. In the fatalities due to CO, the average concentration of CO was 45%. The burning of cellulose mate rial resulted in nothing but the re lease of CO. In the mouse study with exposure to burning building mate rials, the ECG abnormalities were recorded before the smoke from the burning materials was evident. In regard to the harmful properties of PVC to mice, as well as those from polyurethane, polysterene, and phe nol, the pathologic effects of the gases, rather than those of the smoke, appeared first, as shown by atypical ECG changes. It requires less CO in combination with HC1 to cause death. In conclusion, HC1 and CO have a re ciprocal, potentiating adverse efTcct. EFFECT OF SMOKE Smoke is a suspension of small par ticles in hot air and gases. It has a particulate fraction and a gaseous fraction. The particles consist of car bon and are coated with combustible products such as organic acids and al dehydes. The gaseous fraction has an extremely variable composition. Car bon monoxide and carbon dioxide are always present and constitute the bulk of this fraction. However, a wide variety of other toxic gases are present at the scene of a fire. These may be formed by the combustion process or leak from com mercial processing or storage equip ment. The particulate and gaseous fractions combine to exert a large space-occupying effect and can fill an enclosed space at the expense of air. The gaseous fraction of smoke is much more dangerous to life than the particulate fraction. The nose, mouth, and throat, which filter out and trap the particulate fraction, cannot filter out the toxic gases. These gases enter the upper respiratory tract and lungs freely when inhaled. Damage to the lungs may result from exposure to a group of gases and vapors called pul monary irritants (chlorine, phosgene, nitrogen dioxide, sulfur dioxide, and ammonia). On entering the lungs, these agents react chemically with water to produce strong acids or al kalis. A violent inflammatory re sponse occurs, causing destruction of lung tissue. Fire fighters and victims of fires in homes, offices, and industrial com plexes are exposed to smoldering and 394 JAMA, Jan 26, 1976--Vol 235, No 4 Polyvinyl Chloride--Over X CUSAROSS 00814 burning plastics and synthetics ,.m furniture, floor and wallcoverings, textiles, and building materials. Many plastics produce large volumes of pulmonary-irritant gases when burned. Polyvinyl chloride is used ex tensively in furniture, both in the foamed plastic stuffing as well as the covering. Burning 450 gm of this ma terial produces 320 gm of chlorine, phosgene, and HC1, all of which are strong pulmonary irritants. In all, there are 75 known products of PVC degradation. Practically every struc ture today contains plastics capable of producing lung-damaging gases when burned. Therefore, the fire fighter faces a great, new risk in al most any fire. It became obvious that a particular pattern was emerging in which cer tain fire situations were productive of insidious and unpredictable fire casu alties. The lethal chemical smoke was determined to bo HC1 resulting from the decomposition of PVC plastic used in telephone cable and electrical equipment installations. We have found electrical and tele phone cable fires to he especially haz ardous to the fire fighters, due to the toxic gases produced. We have found that when a short circuit developed in a main switch, usually located in a sulv-basement or penthouse of an of fice building or apartment house, the area was always poorly ventilated, and the plastic-covered switches quickly heat to temperatures in ex cess of 93.3 C. The heated conductors cause the plastic insulation to decom pose and emit white, mist-like HC1 fumes that resemble steam. When the temperature range of 232 to 321 C is attained, the gas may he invisible. The fire fighter may be fatally de ceived if he docs not know plastic-cov ered cable is involved in the fire he is fighting. OVERHAUL PHASE The period of time just after the fire is extinguished is termed the "overhaul phase." This is when the fire fighters clean up the foreground. Toxic smoke and fumes are still heing emitted. This is a serious time for toxic gas inhalation to occur since many fire fighters remove their selfcontained breathing apparatus dur ing this phase. Another special hazard during this phase is the "heat sink," ie. concrete that retains a great amount of heat and releases fumes throughout the overhaul phase. Our testing has shown highly toxic con centrations of HC1 in this concrete for as long as one hour after the fire has been extinguished. FUEL LOADING In the late 1960s, the type of "fuel loading" in office and high-rise build ings (ie, contents of the buildings) changed significantly and initiated a new awareness. The noncomhustihle buildings were not burning, hut fur niture within them, huilding insula tion, ceiling tile, wall paneling, and decorations made partly or wholly of plastic were fueling disasters. While a building may he con structed of fire-resistant elements, there is no control over the combustihle material that an individual may elect to bring into the structure. This is the "fuel load" and may he ex pressed as kilograms of eomhustihle material per square meter of floor area. Large differences exist in com bustibility, smoke, anti toxic gas re lease among different eomhustihle materials. More than 50 sq m of red oak, all hurning at its maximum rate, would he required to produce the same rate of smoke as 2.5 meters of acrylonitrile-hutadiene-styrene plas tic pipe. A fire of plastic materials de velops extremely high temperatures because plastics possess a heat of combustion 2' times that of other combustibles. Therefore, the fire would magnify the normal problems of radiant heat, structural damage, and exposure. The fire would exhibit a very high hurning rate hecause the flammability of plastics is much higher than that of other combus tibles. The four most common plastics pro duced in the United States in the past few years are polystyrene, polyethyl ene, polypropylene, and PVC. A chlorethylonc polymer is a plastic solid marketed under a variety of trade names, and currently heing manufac tured at a rate over 8.3 billion kilo grams annually. Polyvinyl chloride (Fig 2) is a plas tic solid widely used as a rubher sub stitute and as electric and telephone wire and cahle covering. It is also uti lized frequently in electrical fixtures, plastic drains, as well as waste pipe Fig 2.--Polyvinyl chloride. for interior plumbing, pliable thin sheeting, film finishes for textiles, "noninflammable" upholstery, rain coats, tubing, belting, gaskets, shoe soles, disposable unbreakable plastic bottles, packaging materials, auto mobile and aircraft seatcovcrs, cor rugated fence toppings, tarpaulins, shower curtains, phonograph records, plastic trays, baby pants, toys, cur tains, and office copying-machines. It is used as an exterior finish in many vehicles, including buses and subway cars, hecause of its high resistance to wear and soiling. When PVC is heated to 225 C, noth ing happens. When heated above that, up to 475 C, PVC does not burn. The combustion range or flame point is 475 C. Between 225 C and 475 C, PVC loses over 60% of its weight. During this process, it thermally de grades and HCI is released. Four hun dred fifty-three grams of PVC at deg radation releases 320 gm of chlorine, phosgene, and HCI. The individual toxicity factors of phosgene and the other major decom position products of PVC, ie, benzene, toluene, total xylenes, naphthalene, and vinyl chloride, are very small, compared with the toxicity factor of HCI. Further, the total or additive toxicity factors of these minor compo nents are also very small in compari son with HCI toxicity. Unfortunately, very little is known about the syner gistic effects of toxic gases (ie, the ability of one chemical to increase or decrease the toxicity of another). The main toxic risks from the decomposi tion products of PVC arc HCI and CO.- Stone et al" elucidated the nature of smoke aerosol and its role in the transport of toxic gases in fire situ ations. They confirmed the fact that the toxic gas, HCI, is adsorbed on soot aerosol. Possible inhalation hazards of such soot are positively related to the size of the soot particles and particle agglomerates. It has been shown that JAMA. Jan 26. 1976-Vol 235. No 4 Polyvinyl Chloride--Dyer & Esch 395 CUSAROSS 0081 the amount and location of particle deposition in the respiratory tract de pends on the particle size.* On inhala tion, soot aerosols would enter the lower lung region and, to an extent, be retained there. Soot particle clus ters, with sizes ranging from 0.1ft to 2.5ft in diameter, would be retained in the alveolar sacs to an extent of from 20% to 40% of those particles inhaled/' At a breathing rate of 18 liters/min for an exposure of one hour, a max imum of 0.7 gm of soot bearing 13 mg of loosely bound HC1 would be re tained in the lower lungs. The effect of HC1 in the gas phase is largely limited to irritability, mainly affecting the upper respira tory tract, whereas loosely bound HC1 condensed on soot aerosol gains ac cess to the lower lungs. Experiments have shown that water droplets of respirable size rapidly adsorb HC1 from the gas phase and approach equilibrium concentrations in frac tions of a second/ SMOKE INHALATION Respiratory distress may develop in fire fighters or fire victims immedi ately or within one to two days of ex posure to combustion products. The best protection against these agents is the mandatory use of the self-con tained breathing apparatus by every fire fighter. When anyone without a breathing apparatus is exposed to more than a few breaths of "choking smoke" characteristic of burning or smoldering plastics, he should receive prompt medical attention. Prior to our investigation, we con sidered most foreground pulmonary casualties to be due to "smoke inhala tion" or CO poisoning. Carbon mon oxide had long been considered the leading cause of death and pulmonary morbidity in fires. Though CO is not noxious and does not actually cause serious pulmonary injury, the amount of CO in a patient is a good indicator of whether more harmful gases are present. Before the introduction of massive fire loads of combustible and ther mally decomposable plastic products, fire surgeons usually considered the CO victim to be "home safe" in four hours after exposure due to the fast half-life of CO in the blood. After ex posure to plastic degradation prod ucts, a period of one to six hours elapses between exposure and onset of severe respiratory and chest symp toms. Treatment is most effective if given during this quiescent phase. Once the symptoms of difficult breathing, cyanosis, or other symp toms, as noted in the reported case, have appeared, it may be too late to prevent severe morbidity or even mortality. The "overhaul phase" after the fire is extinguished is dangerous with respect to fumes also. A Harvard research team headed by Donald P. Dressier, MD, reported in 1973 that when burned, plastics and modern fibers produced colorless, odorless fumes that quickly displace oxygen and cause a dramatic rise in the C02 level of the atmosphere/ Therefore, a person either dies or is rendered unconscious in the early stages of a fire involving these mate rials. If he is unconscious, he soon dies of other lethal fume inhalations." Tests performed in Cambridge, Mass, showed that fire fighters were proba bly affected adversely by the high level of C05 rather than by the initial release of toxic gases." In establishing the importance of detecting the presence of certain toxic gases, the difficulty in detecting CO has been emphasized.'1 Some hu man response mechanisms are more sensitive than others to CO inhala tion." Fairly high levels of CO affect a human's vision, but even higher levels do not affect his sense of timing. A re search team headed by R. A. McFar land, MD, of Harvard University, found that when CO replaces 11% to 17% of the blood's normal oxygen, the peripheral vision is affected and the subject has difficulty viewing stimuli at a 20 angle from the line of sight/ The Harvard team also found that at a 17% concentration of COHh, some subjects had a momentary lapse of at tention and failed to respond to all the stimuli presented. This is impor tant in disproving the once-held con cept that once an individual has de tected the sharp odor of HC1 he can walk away. It has been our observa tion that the fire fighter cannot es cape the HC1 fumes. Cornish and Abar reported that CO and hydrochloric acid were the major toxic products from the combustion of PVC.' They pyrolized PVC polymers in a stream of air by gradually in creasing the temperature from am bient to 600 C. Exposure to this air stream supplemented with oxygen produced pulmonary and interstitial edema in rats. Some of these animals also showed focal bronchial and intraalveolar hemorrhage. In a sealed environment (such as a centrally air-conditioned house, of fice, high-rise unit, or hospital), fumes from plastic degradation could kill, even if the fire is brought under con trol. It has been observed that a sleeping person needs an estimated 12 to 15 minutes to awaken, react to danger, and take appropriate action to save himself. With inhalation of fumes from burning plastic, he will not have that much time. COHb LEVEL AND CIRCULATION As noted by E.P. Radford (writ ten communication), 43 deaths due to fire demonstrated that a blood COHb level of over 65% is nearly always lethal due to the depression of res piration and circulation. Ventricular fibrillation from acute myocardial hy poxia induced by a rapid rise of the COHb level in individuals with a restricted coronary circulation was found to be the likely explanation of a lower terminal blood COHb level. These individuals were found to have severe, preexisting coronary vascular disease. We believe that any compromise of the coronary circulation, eg, ath erosclerosis such as found in the fatal case, would be potentiated by highly irritating chemical fumes. We also believe that other pyrolysis products, especially HC1, have contributed to ventricular fibrillation since its con centration is comparable to that of CO in real fire situations involving plastics. Kishitani has demonstrated that chlorine affects the myocardium more rapidly and more severely than CO. Carbon monoxide may cause changes in enzyme activities suggestive of myocardial damage. Hydrogen chlo ride has been found to be a more po tent myocardial irritant whose ef fects may be difficult to determine by clinical observation. This is in con junction with the development of pul monary edema over a 24-hour period following exposure to HC1. This fur ther complicates and compromises coronary artery oxygen saturation. This could lead to sudden death syn 39 JAMA Jan 26. 1976-Vol 235, No 4 CUSAROSS 00816 Polyvinyl Chloride--Dyer & Esch drome, similar to that in the reportev case. Although in the cases of CO poi soning noted by G. Gordon, (written communication) the ECG changes did appear late if at all and the COHb varied in individuals at the same fire as well as in different fire situations, it has been our experience that all fire fighters exposed to PVC do mani fest ECG signs of its toxicity. There are variable levels of its toxic effect on the lungs, mucous membranes (tra cheal peeling effect), eyes, and other parts of the body. CLINICAL STUDY In'Washington, DC, a clinical study of fire fighters suspected and later known to have been exposed to toxic products from thermal degradation of PVC was conducted by the DC Board of Police and Fire Surgeons between January 1970 and September 1975. One hundred seventy individuals were exposed from one to four differ ent times to these products and re ported two or all of the symptoms of acute toxicity, ie, pain in the anterior aspect of the chest, neck and throat pain, dyspnea, severe headache, dizzi ness, and irregular pulse within a few hours after exposure. Initial physical examinations were performed by the fire surgeon on the fireground, in the hospital emergency room, or at the Police and Firemens Clinic. Laboratory studies including complete blood cell count, determina tions of serum glutamic oxaloacetic transaminase, blood urea nitrogen, or creatinine, and a complete urinalysis were done. Electrocardiograms were performed initially when there was chest pain, extrasystolcs, or cardiac arrhythmia. However, ECG studies were not incorporated as part of the physical evaluation until the latter part of the study when their impor tance was appreciated. About one fifth of the fire fighters had extrasystoles during the first few hours after exposure. Fourteen of the 1. Lowery R: Injury Control at Heavy Service Electrical Fires, safety bulletin. City of New York Fire Dept, September 1969 2. Lee T: Smoke Analysis of Specimens Sub mitted by Fire Marshal Clark of Prince Georges County, Maryland, US Dept of Commerce, Sept 25, 1969, 3. Sax NI: Dangerous Properties of Industrial Materials, cd 3. New York, D Van Nostrand Co Inc, 1968, p 883. 4. Kishitani K: Study on injurious properties last 26 firemen exposed had prema ture ventricular contractions. Some have had recurrence of extrasystoles within the subsequent year. Chest xray films were done at the initial examination and have remained nor mal. Serum electrolyte and arterial blood gas determinations were per formed on 12 of the fire fighters who were more acutely ill, or required hos pitalization. Because of the excellent clinic facilities provided by the Dis trict of Columbia government, all fire fighters were observed in a holding area after exposure and examined at the clinic or the hospital emergency room after transportation from the fireground. Twelve men were ad mitted to the hospital for treatment. If symptoms did not worsen over the first 24 hours in the hospital, they were released and followed up on an outpatient basis at the clinic. Specific treatment, including oxy gen given intranasally at 5 liters/ min, bronchodilators, antihistamines, and decongestants in oral suspension, has been utilized in controlling most of the acute respiratory symptoms. Steroids were given intravenously to three of the fire fighters during hospi talization due to the severity of their signs and symptoms of respiratory distress. Initial and follow-up liver function tests have remained normal in all of these patients. There has been no di rect correlation between severity of symptoms and history of cigarette smoking. None of the fire fighters has had to retire for permanent airway dis orders, Serial studies and follow-up examinations will continue. Since the onset of this study among " profes sional fire fighters, the use of the selfcontained breathing apparatus has been required at all fires where toxic fumes could he present. This is neces sary during the "overhaul phase" also. We urge all physicians to advo cate restriction of unsupervised use References of combustivc products of huildinx materials at the initial sta^e of fire. J Farnlty of Engineering University Tokyo (Bl 31 1-35 (No. 1) 1971 5. Woolley WD: Decomposition products of PVC for studios of fires. Br Polymer J 3 186-193, 1971. 6. Stone JP, Haalett RN, Johnson JE, et al. The transport of hydrogen chloride by soot from burning polyvinyl chloride. J Fire Flammahility 4-42-51, 1973, 7 Stone JP: Transport of hydrogen chloride oi ,-VC products. Fire research activ ity should be maintained at a na tional level to continue study as well as preventive measures for HC1 tox icity in PVC fires. CONCLUSIONS Hazards of Plastic Fires.--Respira tory distress may develop in fire fighters and fire victims after expo sure to combustion products. The complexity of the problem is empha sized when it is recognized that the thermal degradation of PVC results in the formation of at least 75 identi fiable potentially toxic compounds. Three characteristics of plastic fires are the extremely high temperatures, very high burning rates, and thick toxic smoke. The main danger to ex posed fire fighting personnel at the fireground results from the massive formation of HCI gas, and in many instances, Its adsorption on spherical soot particles that are carried into the victims' respiratory tracts. Prevention.--The mandatory use of the self-contained breathing appa ratus hy all who will be vulnerable to toxic smoke will aid in the prevention of plastic fires. Control of hazardous huilding designs, including equip ment and ventilation is also neces sary. Protection by masks during the "overhaul phase'' should be required. Sophisticated air-sampling tech niques are required for definitive study, including gas chromatography. Electrocardiographic studies utilizing base line tracings directly after HCI exposure are stressed. Areas of Future Study.--All atmo spheres should be suspected by the fire fighter. There should be a search for an effective gas analyzer that can immediately assess gas concentra tions released by burning or smolder ing plastics. Further definitive car diologic studies are indicated. The term "smoke inhalation'' should be abandoned and replaced by "inhala tion of toxic combustion products." hy water aerosol in simulated fire. J Fire Flammability 2:127-138, 1975. 8. Fibers, plastic fumes cause smoke deaths, editorial- Ini Fire Fighter 55.8, 1973. 9. Medical tribune report: Human response mechanism may vary in carbon monoxide sensi tivity Med Tribute Nov 8, 1972, pp 15-16 10. Cornish H, Abar E: Toxicity of pyrolysis products of vinyl plastics. Arch Environ Health 19.15-21, 1969. JAMA, Jan 26. 1976-Vol 235. No 4 Polyvinyl Chloride--Dyer & Esch 397 CUSAROSS 00817