J. Mann Prøv at slappe lidt af og så kravl lidt ned af din pind makker, først så tænkte jeg ikke videre over din post og grinte bare af den fordi det er jo total til grin.
Så flipper du total ud over at der bliver stillet spørsmålstegn ved din idioti, du har ingen dokumentation for det du laver og du har tydeligvis ikke sat dig en skid ind i hvad du laver.
Som du selv nævner er dine kilder en makker og en bums, om det så er en og samme person ved jeg ikke, men du ved dog at cellofan er lavet af cellulose fibre og evt. bomuld.
Jeg har så lige brugt den øverste etage og gik lidt dybere ind i det, end at læse en wiki om det. For hvis hvis man skal tegne det så groft om som cellulose og bomulds fiber, kan man lige så godt bruge en reklame eller et par slitte jeans og sy sig en joint.
Lad os derfor kigge lidt på hvordan produceres disse produkter, det er altid meget mere intresant og se på hvad for noget kemi de har stoppet i de der plante fibre for at få dem gemmesigtige og for at have den struktur som matrialet har. Det var ikke nemt med cellofan for efter lidt research og et par opkald, fandt jeg ud af de slet ikke producere Cellofan i DK mere og han mente også at den sidste fabrik i EU var lukket ned i tyskland. (I hver tilfælde for cellofan produktion)
Lige meget det lykkedes mig da at finde lidt om hvilke opløsnings midler de bruger, primært bruges der en væske der heder carbondisulfat (CS2).
Det har ikke været mig muligt at finde ud af hvor meget af dette stof der er tilbage i slut produktet og hvor meget der frigives når produktet brændes, men tager man en hurtig tur med google finder man hurtig ud af at det er noget giftig pis og især i damp/røg form.
Da jeg ikke gider at oversætte det fra engelsk til dansk, paster jeg bare lige lidt tekst jeg fandt om CS2's effekter på mennesker
Citat:
IV. HUMAN HEALTH EFFECTS
A. Pharmacokinetics
1. Absorption - Studies in humans and animals have demonstrated
that carbon disulfide is readily absorbed via the lungs (80%
retention in the first 15 min.) and animal studies indicate
absorption via the gastrointestinal tract. Absorption through
the skin of carbon disulfide in aqueous solution (0.33-1.67 g/L)
was demonstrated in animals and humans, and exposure of the
skin of rabbits to high concentrations of vapor (ò800 ppm)
resulted in measurable absorption (ATSDR 1992).
2. Distribution - In studies with NMRI mice exposed to 35S and
14C- radiolabeled carbon disulfide by inhalation, high levels
of carbon disulfide were present in body fat, blood, lungs,
liver, and kidneys. Much lower levels were found in the brain.
Changes in the distribution of the 35S and 14C radiolabels were
noticeable within one hour of exposure indicating rapid metabolism
of carbon disulfide (U.S. EPA 1986). Other studies with rats and
rabbits reported highest concentrations in lipid-rich tissues,
brain and liver, following inhalation exposure (ATSDR 1992).
Studies with pregnant mice exposed to 35S and 14C-radiolabeled
carbon disulfide by inhalation have demonstrated that carbon
disulfide and its metabolites can pass through the placenta at
all stages of gestation.
Human epidemiological studies have shown carbon disulfide to be
present in the milk of occupationally exposed nursing mothers
(ATSDR 1992)
3. Metabolism - The metabolites of inhaled or ingested carbon
disulfide include thiocarbamide and 2-thio-5-thiazolidinone,
resulting from reactions with amino acids; 2-thioazolidine-4-
carboxylic acid, resulting from conjugation with glutathione;
and thiourea, the probable end product of cytochrome P450
oxidation. These compounds have been found in the urine of
workers occupationally exposed to carbon disulfide (U.S. EPA 1986;
ATSDR 1992).
4. Excretion - Unmetabolized carbon disulfide is primarily excreted
in expired air (10-30% of the absorbed dose) and a small amount
(<1%) is excreted unchanged through the kidneys (ATSDR 1992).
The amount of carbon disulfide excreted through the lungs falls
rapidly after exposure ceases. Half times reported for pulmonary
excretion in rats range from 35 to 85 minutes (U.S. EPA 1986).
The remaining 70-90% of the absorbed carbon disulfide is
metabolized and excreted through the kidneys (ATSDR 1992). The
concentration of sulfur compounds in the urine of rats decreased
to control levels in 12-14 hours following inhalation exposure
to 2 mg/L carbon disulfide for 8 hours (U.S. EPA 1986).
B. Acute Toxicity
Exposure by inhalation or by mouth to moderate to high levels of
carbon disulfide can be fatal to humans. Direct contact with
liquid carbon disulfide can burn the skin and the eye.
1. Humans - Carbon disulfide inhalation can result in local
irritation and pharyngitis and central nervous system effects
(see Section IV.G.1). Slight symptoms have been reported at
doses of 320-390 ppm for several hours. Definite symptoms
appear at 420-510 ppm for 30 min (total dose ÷ 11.9-14.4 mg/kg)
(see end note 3). The symptoms become serious after exposure
to 1150 ppm for 30 min.; dangerous to life after 30 min. at
3210-3850 ppm; and fatal in 30 min. at concentrations above
4815 ppm (HSDB 1994). The oral ingestion of 15 mL (÷300 mg/kg)
carbon disulfide may be fatal to an adult (HSDB 1994). Skin
contact can produce pain and erythema and prolonged contact
produces vesiculation and chemical burns. Contact with the eyes
causes severe chemical burns of the cornea (HSDB 1994).
2. Animals - LD50 values for oral exposure reported in the literature
searched are as follows: rat, 3188 mg/kg; mouse, 2780 mg/kg;
rabbit, 2550 mg/kg; guinea pig, 2125 mg/kg (U.S. EPA 1986).
LC50 values of 25 g/m3 for 2 hours for rats and 10 g/m3 for
2 hours for mice were also reported (RTECS 1994).
C. Subchronic/Chronic Effects
Prolonged inhalation exposure to carbon disulfide can adversely
affect the human nervous system and cardiovascular system.
Prolonged inhalation exposure can damage the nervous system, the
cardiovascular sytem, and the kidney of laboratory animals.
1. Humans - Chronic occupational exposure to carbon disulfide has
resulted primarily in neurological and cardiovascular effects.
Gastrointestinal and immune insufficiency problems have also been
recorded. See Section IV.G.1 for information on the neurological
effects. Exposure to 144-321 ppm (445-1000 mg/m3) for 5 years or
longer resulted in gastrointestinal disturbances in 28 of 100 cases
(U.S. EPA 1986). Cardiovascular effects including increased
blood pressure, changes in ECG, increased plasma triglycerides
and low-density lipoproteins, and increased angina and mortality
from coronary heart disease have been reported following exposure
to 6-32 ppm (18.7-100 mg/m3) for 5 months to over 5 years.
Decreased immunoreactivity was seen after exposure to 3 ppm
(duration of the exposure was not given in the secondary reference)
(U.S. EPA 1986).
Link:
http://www.epa.gov/chemfact/s_carbds.txtNu er jeg ikke plast mager eller ligne, men helt ærligt så tror jeg stadig ikke cellofan er godt og ryge på nogen måde.
Desuden fik jeg også at vide at man ikke rigtig bruger cellulose fibre mere, men nye ploymære forbindelser som har samme egenskaber som alm cellofan. Det er bare billigere at producere, men samtidig 100 % kunststoffer som han mente ville havde samme brænde egenskaber som gammeldags cellofan. Da men jo ikke ville være nemt at markeds føre et nyt cellofan produkt hvis de fabrikker der pakker med cellofan så skal til at have nye pakke maskiner, det lyder nu også meget fornuftig i mine øre.
Jeg vil på alle måder fraråde alle også J. Mann selv i at ryge cellofan joints, minimum indtil der liger nogle klare beviser for at cellofan ikke frigiver giftige stoffer ved afbrænding. Det er ikke alle giftige stoffer der udvikler sort røg, så bare fordi det ikke udvikler en tyk tåge og drypper betyder det ikke at stoffet er helt ufarligt at ryge.
MVH
Piercer :twisted:
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