In a preliminary report of the 19th August 1997, Vinegar and others describe the effects of inhaling refrigerants 1301, 134a and 227ea at the USAF Medical Center, Wright-Patterson AFB, Ohio. The seven human subjects were healthy male volunteers with ages from 21 to 49. All subjects showed no adverse affects when breathing through the apparatus pure air or 0.5% by volume R-1301 in air for 30 minutes and none were expected for R-134a.
After 4.5 minutes of breathing R-134a at 0.4% by volume in air, subject three lost consciousness and both pulse and blood pressure dropped to zero. Medical personnel restored pulse and blood pressure and administered 100% oxygen. Vital signs returned to pre-exposure values after approximately one hour. After 10.5 minutes breathing 0.4% R-134a, subject five's blood pressure and pulse rose rapidly and the exposure was terminated. After one hour breathing room air and then only 2.5 minutes breathing 0.2% R-134a, subject five's blood pressure and pulse again rose rapidly and exposure was terminated. These were the only two subjects exposed to R-134a. Both subjects were still reporting problems with dizziness and balance six weeks after the exposure.
In The Lancet of the 23rd August 1997, Hoet and others describe an epidemic of liver disease in nine Belgian crane drivers. In March 1996, R-114 had been replaced in the air conditioning system of the crane cabin by a mixture of R-123 and R-124. At the end of April one of the drivers became progressively ill and was admitted to hospital with acute hepatitis. At the end of June he returned to work but within a week returned ill to hospital. Another driver developed acute hepatitis in May and a third was admitted to hospital in July. Six additional drivers developed symptoms of hepatitis. An inspection in July revealed a refrigerant leak into the cabin and after repairs in August no recurrences or new cases of liver diseases were recorded. Clinical tests on blood and a biopsy also indicated refrigerant as the cause. Similar disease has been observed in humans exposed to halothane and in animals exposed to R-123. The concentration the crane drivers were exposed to must have been of the order of 0.002% by volume since the leak occurred over four months.
In 1995, a technician in Brisbane Australia accidently exposed for about a minute to an R-134a concentration of about 2% had to recover in hospital. In 1996, a taxi-driver with a slowly leaking air-conditioner in the same city complained of feeling ill, recovered when he took a week off, got sick again when he returned to work and had no further symptoms when the evaporator was repaired.
Hoet and others (1997) suggest that metabolism to trifluoroacetic acid which modifies proteins causes the R-123 disease. Trifluoroacetic acid is also a decomposition product of R-134a but not of R-12 or R-1301 so the suggestion of Hoet and others may explain all the observations above.
The average exposure of refrigeration technicians to R-123 is much less than 0.002%, about 0.0001% and the peak during some procedures about 0.001% (NICNAS 1996). The exposure of car air-conditioner technicians to R-134a may be higher. These refrigerants are odorless so technicians rarely connect refrigerant exposure with any illness which occurs.
Sudden failure of air-conditioner components in car passenger compartments may occur as frequently as once in a million user years for some designs. Failures in cars retrofitted to R-134a could cause compartment concentration to exceed 0.4% by volume for over five minutes (Maclaine-cross 1997). The frequency of small pinhole and fatigue fracture leaks into the passenger compartment is of the order of once in a thousand user years. R-134a is original equipment on most cars manufactured after 1994. The toxicology data above suggests that leaks may cause driver errors resulting in personal injury and property damage.
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