A Report of Occupational Deaths Attributed to Fluorocarbon-113

May, David C.; Blotzer, Michael J.

doi:10.1080/00039896.1984.10545862

Cited by 16 publications

(4 citation statements)

References 9 publications

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“…These studies link arrhythmias to "epinephrine sensitization," in which the myocardium's transmembrane electrical milieu is altered by the halocarbon to become more sensitive to catecholamineinduced arrhythmias. Although many fluorocarbons alone can cause arrhythmias at high exposure levels, some fluorocarbons produce serious arrhythmias in mammals at exposure levels as low as 5,000 ppm, when combined with intravenous epinephrine at tachycardia-producing doses [Reinhardt et al, 19711. There have been several cases of presumed cardiac sudden death with workplace exposure to these chemicals, especially to CFC 1 13 (1,1,2-trichloro-l,2,2-trifluoroethane), and 1 , l , l -trichloroethane [Hatfield and Maykoski, 1970;Jones and Winter, 1983;May and Blotzer, 1984;Lehmann, 1980;Yonemitsu et al, 1983;Clark et al, 1985;NIOSH, 19891. In addition, the widely used fire extinguishing agent, halon 121 1, has caused sudden death when abused for recreation and, most recently, when used to extinguish a fire in a confined space [Smeeton and Clark, 1985;Steadman et al, 1984;Lerman et al, 19911.…”

Section: Subjectmentioning

confidence: 97%

“…Experimental studies in animals have demonstrated these effects at exposure concentrations above permissible exposure levels [Zakhari and Aviado, 19821. Human arrhythmias and sudden death have been documented in cases of occupational overexposure and volatile substance abuse [May and Blotzer, 1984;Ramsey et al, 1989;Lerman et a]., 19911. It is not known whether or not lower exposure levels regularly encountered in the workplace, in concert with exertion, may increase the frequency of arrhythmias and the risk of sudden death.…”

Section: Introductionmentioning

confidence: 99%

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A study of the cardiac effects of bromochlorodifluoromethane (Halon 1211) exposure during exercise

et al. 1992

American J Industrial Med

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Bromochlorodifluoromethane (halon 1211, a fire extinguisher), like other fluorocarbons, has been linked with ventricular arrhythmias and myocardial depression. Ten healthy firefighters, aged 40-50, were exposed to 1,000 ppm halon while exercising, in a double-blind, placebo-controlled crossover experiment, and were monitored during and after exposure. Complex ectopy (ventricular couplets and idioventricular rhythm) occurred in two subjects with halon, but none with placebo. One subject had 49.5 ventricular premature beats (VPB)/hour during the period of halon exposure and subsequent 8 hours and only 8.7 VPB/hour during the same period of placebo. In addition, 8 of the 10 subjects had a smaller systolic blood pressure rise during exercise with halon than with placebo. None of the observed differences was statistically significant. These results are consistent with findings in other investigations, suggesting that occupational fluorocarbon exposures may be cardiotoxic in certain individuals, although the small sample sizes used in this and other studies have resulted in limited statistical power to demonstrate this effect.

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Section: Subjectmentioning

confidence: 97%

Section: Introductionmentioning

confidence: 99%

A study of the cardiac effects of bromochlorodifluoromethane (Halon 1211) exposure during exercise

et al. 1992

American J Industrial Med

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“…No adverse effects were noted in a population of workers exposed to average levels of 700 ppm with peaks to 4780 ppm (Imbus and Adkins 1972;NIOSH 1980). However, deaths of two workers have been reported when individuals have been overexposed to CFC 113, especially in "confined spaces" (May and Blotzer 1984). In one case, the exposure level was estimated to be 128,000 ppm; in the other, it was estimated to have been in the range of 6000-37,000 ppm for 15 min.…”

Section: Acute Toxicitymentioning

confidence: 99%

The development of environmentally acceptable fluorocarbons

Rusch¹

2018

Critical Reviews in Toxicology

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Chlorofluorocarbons (CFCs) were introduced in the 1930s as the safe replacements for the toxic and flammable refrigerants being used at that time. Subsequently, hydrochlorofluorocarbons (HCFCs) were also developed. In addition to refrigerant applications, they were used as foam blowing agents, as solvents and as propellants for many aerosols. In the 1970s and 1980s, concern developed about their environmental impact, specifically on stratospheric ozone depletion. Industry began to consider acceptable replacements. In 1987, many of the governments of the world came together and drafted the Montreal Protocol, calling upon Industry to initially phase out production of the CFCs and later HCFCs. Within 4 months of the signing of the Montreal Protocol, the 15 global major producers joined together to form the Alternative Fluorocarbons Environmental Acceptability Study (AFEAS), which sponsored research into environmental effects and the Program for Alternative Fluorocarbons toxicity Testing, PAFT), which examined the toxicology of potential replacements for the CFCs and HCFCs. Nine replacements were identified by companies and, through this international cooperation; toxicology programs were designed, conducted, and evaluated without duplication of effort and testing; consequently these new products were introduced within less than 10 years. Indeed the Montreal Protocol has been recognized as the most appropriate international treaty to phase-down HFCs. In 2016 the Kigali Amendment to the Montreal Protocol set out a phase-down schedule for the consumption and production of HFCs. In order to reduce the consumption and emissions of high GWP HFCs. Recently lower GWP HFCs and very low GWP HFOs (hydrofluoroolefins and HCFOs (hydrochlorofluoroolefins) have been introduced into a range of applications. Summaries of the toxicology profiles of some of the original CFCs and HCFCs, the replacements and the new post-PAFT replacements are described.

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“…Although sudden occupational deaths among Freon 113 workers have been reported (May et al, 1984;Clark et al, 1985;Yonemitsu et al, 1983;, the cause of death still remains to be solved. A common feature of these industrial cases was hypoxia caused by Freon 113 accumulation at work sites since the gravity of Freon 113 is 6.47 times higher than air (May et al, 1984). Thus, in some reports , the cause of sudden death was ascribed to asphyxia.…”

Section: Introductionmentioning

confidence: 95%

Enhanced Arrhythmogenicity of Freon 113 by Hypoxia in the Perfused Rat Heart

1990

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The interaction of Freon 113 (1,1,2-trichloro-1,2,2-trifluoroethane) and hypoxia on the heart conduction system was studied using electrocardiogram monitoring of isolated perfused rat hearts. Freon 113 (0.2 mM) alone elicited significant atrioventricular conduction delay (p less than 0.05) and heart rate decrease (p less than 0.01), which were significantly enhanced by hypoxia (75% oxygen decrease), for instance, resulting in 2:1 AV block. The data suggest that arrhythmogenicity of Freon 113 on the heart conduction system may be enhanced synergistically by hypoxia.

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A Report of Occupational Deaths Attributed to Fluorocarbon-113

Cited by 16 publications

References 9 publications

A study of the cardiac effects of bromochlorodifluoromethane (Halon 1211) exposure during exercise

A study of the cardiac effects of bromochlorodifluoromethane (Halon 1211) exposure during exercise

The development of environmentally acceptable fluorocarbons

Enhanced Arrhythmogenicity of Freon 113 by Hypoxia in the Perfused Rat Heart

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