[ Previous ] [ Next ]

OTHER ALDEHYDES  (there are many) include:

                Cinnamic aldehyde  reported to be a skin irritant, sensitiser and urticariogenic agent;          Acetaldehyde results in eye irritation and respiratory discomfort.  (Alcohol converts to acetaldehyde via the enzyme alcohol dehydrogenase, in the body); 

                Acrolein  (or  acrylaldehyde, acetic aldehyde, acetic ethanol,  ethanal,  methyl formaldehyde, propenal, ethylene aldehyde, magnacide, biocide, slimicide)  causes severe pulmonary irritation, lacrimation (used in WW1 as "Papite" tear gas), and tissue damage, elevated liver alkaline-phosphatase etc.  (Pinnas JL, Meinke G C, Hazardous Materials Toxicology...1992, 981-985).  Acrolein is very reactive.  Human poison by inhalation and through skin.  Human mutagenic data.  Used as component of military poison gases, herbicide, algicide for water treatment, fungicide, bactericide, to modify food starch, liquid fuel...  Produced in large amounts by overheated cooking oils and animal fat.  A major contributor to the irritative quality of smoke and petrochemical smog.

[1]  Metaldehyde  is used on slugs and snails. Also a fuel for small heaters.  Poisoning in children from eating it results in nausea, vomiting , fever, muscular rigidity, twitching ... convulsions, liver and kidney damage, coma, death from respiratory failure.

[2]  Peraldehyde

Aldicarb (2-methyl-2-{methylthio} propionaldehyde O-{methylcarbamoyl} oxime) is one of the most potent pesticides.(EPA)

(3)   ANAESTHETICS

 "Principal health concerns regarding occupational exposure to anesthetic gases are carcinogenicity, neurobehavioural effects, reproductive effects, interference of nitrous oxide with vitamin B12 metabolism [can cause neurologic abnormalities with chronic heavy exposure], and potential renal and hepatic effects."

[3]  These volatile chemicals/drugs inhaled include: ether, chloroform, ethylene, nitrous oxide, cyclopropane, halothane, enflurane, isoflurane, sevoflurane, desflurane. Occupational hazards related to waste anaesthetic gases were recognised in the 1970s and '80s.  Some are readily soluble (ie easily absorbed in solution - blood) eg halothane, enflurane, and isoflurane, or poorly soluble eg nitrous oxide.  Only when blood saturation occurs does the drug begin to exert a partial pressure and have an effect; a poorly soluble drug rapidly produces effects.  In people with high cardiac output there is rapid delivery of the drug to body tissues where the drug moves out of the blood across tissue membranes.  Highly perfused tissues (vessel-rich groups - VRGs)  include the brain, heart, kidneys which get 75% of cardiac output.  Poorly perfused tissues make up 75% of body mass but get 25% of cardiac output - they have delayed uptakes of anaesthetic agents.  Elimination from skeletal muscle and fat will correspondingly be a much slower process. All inhalation agents are respiratory depressants.  Current theories suggest that inhalation agents interrupt neuronal activity in the central nervous system and may depress excitatory transmission or may prolong inhibitory transmission.

[4]   Professor William Rea, cardiothoracic surgeon, (and subsequently Director of the Brookhaven Environmental Control Unit, Dallas, Texas) attributes his chemical sensitivity to exposure to anaesthetics and fumes from the heart lung machine (motor exhausts and plastics) "in other words, chlorinated hydrocarbons", working in theatre Mon-Sat.  He describes his symptoms: headaches gradually getting worse, periods of fatigue, a lot of muscle aches, irritable colon, sore throats all the time, recurrent sinus, flu-like symptoms until his wife said "no-one can have flu 365 days a year."

[5]    Anaesthetics used in Nelson Hospital, NZ  at the time of maximum glutaraldehyde exposure included nitrous oxide, halothane, isoflurane, sevorane.  Anaesthetics at Whangarei Hospital were:nitrous oxide, fluothane (halothane), isoflurane, ethane, cycloprane (very rare), CO2.

                Ether, the first general anaesthetic, 1846;  excessive use damages the central nervous system. Very flammable (as is cyclopropane).

[6]    Nitrous Oxide  (used about 1860 on) or laughing gas also used in commercial products eg whipped cream and cooking oil sprays.  It "acts to potentiate most volatile anaesthetics".

[7]    Used without sufficient oxygen can cause irregular heart patterns, brain damage, headache, cerebral edema, death. "Because it is administered in high concentrations, pollution levels are much higher than for the halogenated anaesthetics...". Nitrous Oxide interferes with the formation of one of the essential bases in DNA but there are no clear answers on fetotoxicity or neurological disorders.

[8]    Exposures in dental operations may be excessive and more difficult to control than in theatre, and dental workers may suffer adverse reproductive effects, decrease in mental performance, audiovisual ability, manual dexterity (NIOSH Alert, 1994).  "Memory which is one of the most recently developed functions of the brain, is highly susceptible.....experimental evidence shows nitrous oxide affects the behavioural performance in concentrations as low as 50 ppm".

[9]    Chloroform  1831, was the first halogenated hydrocarbon solvent anaesthetic. It depresses respiration and acts directly on the central nervous system. (Halogens are the chemically-similar chlorine, bromine, iodine, fluorine which form salt-like compounds with sodium and most metals.)  Its use has been abandoned because of dose-related toxic effects on the liver. Chloroform produces active free radicals during biotransformation by the cytochrome P-450 system.

[10]    Also causes heartbeat irregularities and damage to the kidneys.   Chronic low levels of  chloroform may still be found in some municipal water supplies.

11]     Halothane  (Fluothane - a bronchodilator.)  Used since the 1960s, probably still the most widely used in the world though isoflurane is generally used in UK and USA. Halothane is in essence halogenated ethane (enflurane and isoflurane are halogenated methyl ethyl ethers). Chronic exposure said to lead to nervous system toxicity and behavioural changes. Issues of reproductive toxicity have been more or less discounted.  Renal toxicity is dose related and immunological toxicity is less clear. The main danger is hepatotoxicity (liver..).

[12]    The 1974 survey by the American Society of Anesthetists found increased self-reported liver disease in male and female operating room  (OR) nurses, but what was attributable to anesthetics is unknown. (Reported in Suruda, p632). 24 resident doctors were compared at work before (control) and after 3-4 hrs of halothane exposure, and after 3-4 hrs of non-halothane (thio-O²-N²O) exposure.  Testing  in the non-halothane group showed depression of motor skills by 5.5% and memory by 17%. Testing in the halothane group showed reduction of motor skills up to 27% and memory 45% compared to the control group. Levels of halothane were estimated up to 26ppm.  (Another study showed halothane affected  motor ability in concentrations as low as 0.2%.  Similarly trichloroethylene and cyclopropane).  "Memory is a function susceptible to even the lowest concentrations of anaesthetics." (Another study showed enflurane causes no such change.)  "Halothane can be traced in the breath of anaesthetists up to 64 h after cessation of exposure." All reported in Malhotra

[13].     Enflurane  (Ethrane) is a vasodilator acting directly on smooth muscles.  Extremely lipid (fat) soluble; may have prolonged action in obese individuals. Lipid soluble drugs rapidly move across tissue membranes. Isoflurane (Forane) widely used - has a stabilising effect on the cardiovascular system.  Less soluble in blood than halothane therefore recovery more rapid.

[14]      Desflurane has lower blood and body tissue solubility therefore its uptake and elimination is faster. It undergoes minimal metabolism and should have low potential for toxic effects. Exact mechanisms for anaesthesia are not known but volatile anaesthetics have very specific actions at the molecular level with protein receptors  rather than surrounding lipid membranes being principal targets.  Halogenated anaesthetics depress neuromuscular function and increase the potency of neuromuscular blocking drugs in a dose dependant manner.  (1994 information).

15]    (Local anaesthetics are all related to cocaine and no two have the same effect "depending on the person's physical make-up".)

[ Previous ] [ Next ]