ANSWERS: 25
Non Contact Infrared Thermometer -- $19.99
While Supplies Last
13deals
Ad
  • Likely not. Though marijuana and tobacco smoke are virtually identical (see report below), marijuana users generally consume far less than tobacco users. Typically, a tobacco user will consume more than 10 tobacco cigarettes a day, while a marijuana user will consumer one marijuana cigarette a day or less. There are exceptions, but generally speaking, marijuana users consume less than tobacco users. As a result, marijuana users will have fewer lung problems (or at least to a lesser degree). Strictly speaking, however, inhaling any burning substance in to your lungs will cause pulmonary irritation, which could lead to adverse respiratory symptoms. Huber, G.L. et al, "The Effects of Marihuana on the Respiratory and Cardiovascular Systems," pp 3-18 in G. Chesher et al (eds), Marijuana: an International Research Report, Canberra: Australian Government Publishing Service (1988). [Added in response to James Edwards] The length of time the smoke is held in the lungs is irrelevant since most marijuana users smoke less marijuana cigarettes than tobacco cigarettes consumed by tobacco users. As I mentioned above, on average tobacco users smoke ten times more cigarettes than marijuana users. If you still do not agree with me, feel free to read the work cited above for more academic information on the issue. Don't rate something negative in retaliation for a negative rating you have received.
  • Smoking a marijuana cigarette is the equivalent of smoking about ten regular cigarettes, and if you're speaking of smoking marijuana out of other devices (like a bong, per say), you have to understand that you're taking in a lot more smoke, much more quickly, and the body (especially the lungs) have little defense when that much smoke is being pushed through (in, whatever) them.
  • Much more harmful in many ways. When someone pulls on a cigarette, they take a drag. When someone takes a hit off a joint or blunt then they are taking alot bigger drags. Also pot creates a much harsher resin that is thick enough to use as superglue. When you take a bongrip- you are essentially forcing so much of this dirty smoke down your lungs and then try to hold it in to maximize the level of thc intake. The same thing with taking shotguns. Also when people tell you about all the chemicals in cigarettes versus marijuana it is a very biased opinion. We know about the chemicals in cigarettes because they are legal and consistant with how they are made. When it comes to pot it could have been laced with anything. I know of several different instances where the dealer laced it with a little crack to get his clients addicted to his pot. That is where the term "ses blunt" came from. Also dealer lacing it with embalming fluid- " heni blunt", laced with cocaine- is the "chronic or primo". Also they have put things on to pot to intensify the smell such as a little ammonia will intesify the smell to make it smell better or stronger, but too much will make it smell like ammonia - obviously. Another thing to consider is that 9 times out of 10, most people who smoke weed usually smoke cigarettes as well. There are few exceptions. There are also the pesticides and fertilizers used to help them grow. A pot plant is probably one of the most loved plants by bugs and other creatures. Most plants do better in their natural habitat but pot does the best with hydroponics. Now i know what a lot of stoners are thinking if they are reading this part. If you grow it yourself then you dont have to worry about it being laced. That is very much correct. You do have to worry about the fact that the more potent the pot is, the worse it is for your body. Marijuana definitely will always do more harm then good. It makes you cough, crave junk food, lazy and unmotivated, and worse it puts you in the enviroment of illegal activity and harder drugs. Hence the term the gateway drug. Not because you want a better high, but the fact that you are now mixed up with the crowd of people who are doing things they know they shouldnt. Iam sure there is a stoner out there who would disagree with me though. The fact of the matter is that every crackhead and coke addict started with some pot. Some folks will say that this needs to be supported by research, but with a little brains they would realize that it would be a waist of time, effort, and money to even do research on something to simply state the obvious. If they do disagree then most likely they are a smoker of the marijahoochie. So it seems very irrelavent as to whether they breathe oxygen or not. It would be foolish to think that some poor fella actually smoked crack before pot, but hey this is getting into something that has nothing to do with the questions.
  • I personally do not have any idea which is more harmful for your lungs, all I know is that both are harmful to inhale. Here's a quick reference that helps support Ryan Gurnetts agrument (that is that marijuana is more harmful) Wu, T. C.; Tashkin, D. P.; Djahed, B.; and Rose, J.E. Pulmonary hazards of smoking marijuana as compared with tobacco. New England Journal of Medicine, 318: 347-351, 1988. However this is from 1988 and I'm sure there are more current reports that both agree and disagree with their conclusion "that smoking marijuana, regardless of tetrahydrocannabinol content, results in a substantially greater respiratory burden of carbon monoxide and tar than smoking a similar quantity of tobacco." The report does not support the claim made by Ryan Gurnett that 1 joint is equal to 10 tobacco cigarettes. It however does argue that that someone who smokes five joints per day MAY be taking in as many cancer-causing chemicals as someone who smokes a full pack of cigarettes every day. Note the MAY. Hope this helps you on your way to finding out which is more harmful.
  • Heres some info that might help you get an answer for your question. Someone who smokes marijuana regularly may have many of the same respiratory problems that tobacco smokers have. These individuals may have daily cough and phlegm, symptoms of chronic bronchitis, and more frequent chest colds. Continuing to smoke marijuana can lead to abnormal functioning of lung tissue injured or destroyed by marijuana smoke. Regardless of the THC content, the amount of tar inhaled by marijuana smokers and the level of carbon monoxide absorbed are three to five times greater than among tobacco smokers. This may be due to the marijuana users inhaling more deeply and holding the smoke in the lungs. This segment can be found at: http://www.marijuanaaddiction.info/effects-of-marijuana.htm
  • Cigarettes are proven to be worse for you than Marijuana1) Most marijuana smokers smoke the bud, not the leaf, of the plant. The bud contains only 33% as much tar as tobacco. 2) Marijuana smokers do not smoke anywhere near as much as tobacco smokers, due to the psychoactive effects of cannabis. 3) Not one case of lung cancer has ever been successfully linked to marijuana use. 4) Cannabis, unlike tobacco, does not cause any narrowing of the small air passageways in the lungs. In fact, marijuana has been shown to be an expectorant and actually dilates the air channels it comes in contact with. This is why many asthma sufferers look to marijuana to provide relief. Doctors have postulated that marijuana may, in this respect, be more effective than all of the prescription drugs on the market. Studies even show that due to marijuana's ability to clear the lungs of smog, pollutants, and cigarette smoke, it may actually reduce your risk of emphysema, bronchitis, and lung cancer. Smokers of cannabis have been shown to outlive non- smokers in some areas by up to two years. Medium to heavy tobacco smokers will live seven to ten years longer if they also smoke marijuana. Cannabis is also radically different from tobacco in that it does not contain nicotine and is not addictive. The psychoactive ingredient in marijuana, THC, has been accused of causing brain and genetic damage, but these studies have all been disproven. In fact, the DEA's own Administrative Law Judge Francis Young has declared that "marijuana in its natural form is far safer than many foods we commonly consume."
  • Techinally yes, in the real world, no. This is a classic question which comes about because of the claims of the ONDCP that 'smoking marijuana is more harmful to your health than tobacco'. It is true at face value but completely inaccurate when logic is applied. The calculation is based on the amount of carcinogenic tar that is absorbed into a sample filter through an artificial 'breathing emulation' device that simulates inhaling and exhaling smoke. The filters are then analyzed for bulk content. Marijuana is far higher in tar, which can be carcinogenic, but lower in carbon monoxide, does not contain cyanide nor ammonia which are potent cytotoxins in cigarette tobacco, nor nicotine, the single most potent carcinogen in tobacco smoke. The claim that marijuana is more hazardous is based on an equal amount of material by weight, therefore - if you smoke two packs a day of cigarettes, you have to smoke 40 cigarette-sized joints to suffer the 'higher health hazard'. Typical daily amounts of heavy cigarette and heavy marijuana smokers might be 10-50 cigarettes and 0.5 - 4 equivalent 'joints'.
  • One reason marijuana smoke is a suspected carcinogen is that marijuana smoke contains polycyclic aromatic hydrocarbons (PAH), which are known carcinogens. A marijuana cigarette typically delivers nanogram quantities of PAHs and microgram quantities of cannabinoids, a unique class of cyclic hydrocarbons. Marijuana smoke is presumed carcinogenic not only because it contains PAHs, but also because cannabinoids, in their own right, modulate cytochrome (CYP1) enzymes required for PAH activation and detoxification. Until quite recently, PAH-related carcinogenicity was attributed to CYP1 involvement with PAH-related DNA damage in vitro, whereas in vivo experiments now suggest a crucial role for CYP1 enzymes in the detoxification rather than metabolic activation of PAHs (Nebert et al. 2004). As competitive substrates for CYP1 enzymes, concomitantly administered hydrocarbons have been shown to prevent the development of tumors that otherwise results from the administration of a single hydrocarbon (Conney 2003). In the same respect, cannabinoids may competitively inhibit the activation of otherwise carcinogenic hydrocarbons (i.e., PAHs). Cannabinoids may also exert anti-carcinogenic effects unrelated to their hydrocarbon structure. Like anti-carcinogenic polyphenols (Ciolino et al. 1998), cannabinoids have been shown to increase levels of CYP1A1 messenger RNA while reducing CYP1A1 enzyme activity through aryl hydrocarbon receptor ligation. Spiking tobacco tar with THC, the primary cannabinoid in marijuana smoke, was shown to markedly reduce CYP1A1 activity (Roth et al. 2001). Another reason marijuana smoke is a suspected carcinogen is that cannabinoid administration promotes cancer in laboratory mice under certain conditions. High systemic doses of cannabinoids have been shown to promote cancer via COX-2 elevation (Gardner et al. 2003) and immunosuppression (Zhu et al. 2000) favoring tumors devoid of cannabinoid receptors (McKallip et al. 2005); overwhelmingly, however, most in vivo studies have demonstrated that cannabinoids  administered either locally or systemically over a range of doses  inhibit cancer (Munson et al. 1975, Kaplan 1984, Chan et al. 1996, Blazquez et al. 2003, Blazquez et al. 2004, Bilfuco et al. 2001, Bilfuco et al. 2004, Casanova et al. 2003, Duntsch et al. 2005, Grimaldi et al. 2006, Kogan at al. 2004, Massi et al. 2004, McKallip et al. 2002, Portella et al. 2003, Recht et al. 2001, Sanchez et al. 2001). A third reason marijuana smoke is a suspected carcinogen is the presence of lesions in the bronchial epithelium of marijuana smokers. Smoking marijuana produces epithelial changes such as squamous metaplasia (SM) and other lesions commonly associated with respiratory exposure to smoke in general (Barskey et al. 1998). On the one hand, SM not only follows exposure to potent carcinogens in laboratory strains of mice, but it also precedes the development of squamous cell carcinoma of lungs (SCCL) in humans. One the other hand, the multiplicity of SM lesions was higher among SCCL-resistant mice (e.g., C57BL/6J = 5.0 - 6.0) than it was among SCCL-susceptible mice (e.g., NIH Swiss = 2.1 - 4.9: Wang et al. 2004); in humans preneoplastic lesions such as SM are generally reversible and often regress spontaneously (Winterhalder et al. 2004). As it turns out, bronchial lesions may have little, if any at all, predictive value. In fact, according to recent findings, "Distribution and outcome of preneoplastic lesions have been found to be unrelated to various risk factors such as smoking... The 54% regression rate of all preneoplastic lesions, 26% to 39% progression rate to CIS/SCC of individuals with lower-grade dysplasia or severe dysplasia with no significant difference in progression rate and time to progression combined with nonstepwise histologic changes unrelated to the initial histologic grading indicate that one cannot differentiate the potentially more malignant preneoplastic lesions among the many preneoplastic lesions present in the bronchial mucosa. The initial WHO classification of any preneoplastic lesion cannot be reliably used for accurate risk assessment of field carcinogenesis" (Breuer et al. 2005). A fourth reason marijuana smoke is a suspected carcinogen is that marijuana tar, much like that from tobacco, was shown to produce benign tumors when painted on the skin of animals (Cottrell et al. 1973); however, tar from tobacco smoke was shown to cause frank malignancies when painted on the skin of animals, whereas that from marijuana smoke was not (Cottrell et al. 1973). Along these lines, subsequent research has failed to establish the carcinogenicity of marijuana smoke in animals. In one study, prolonged exposure to marijuana smoke failed to cause precancerous or carcinogenic effects in monkeys (Talaska et al. 1992). In another study, interestingly enough, exposure to marijuana smoke actually retarded the growth of implanted murine sarcoma (Watson 1989). This inhibition was not related to the cannabinoid content of the smoke. The true neoplastic effects of marijuana smoke might emerge from administration of marijuana-derived chemicals directly to cancers pre-existing in (pulmonary) tissues with the highest exposure to marijuana smoke. Thus far, in vivo studies on the neoplastic properties of cannabinoids have, unfortunately, been conducted with BALB/cJ and C57BL/6J murine strains, which are not susceptible to SCCL. Animal research on smoke-related cancer is problematic because, for example, there has yet to be an animal model in which tobacco smoke exposure causes SCCL. In evaluating the carcinogenicity of any type of smoke, one must remember that it was epidemiology, rather than animal research, that first incriminated tobacco smoke as a carcinogen 70 years ago. More recently, epidemiologic studies  especially those that included a large number of cases and/or randomly selected controls  tend to suggest, if anything, an inverse association between marijuana use and cancers (Morgenstern et al. 2006; Rosenblatt et al. 2004; Ford et al. 2001; Zhu et al. 2002). Marijuana smoke may ultimately prove to be as carcinogenic in humans as some experts claim it to be animals, but it is animal research that serves to elucidate epidemiology, rather than vice versa. Further reading(s): Baek SH, Kim YO, Kwag JS, Choi KE, Jung WY, Han DS. Boron trifluoride etherate on silica-A modified Lewis acid reagent (VII). Antitumor activity of cannabigerol against human oral epitheloid carcinoma cells. Arch Pharm Res. 1998 Jun; 21(3): 353-6. Barsky SH, Roth MD, Kleerup EC, Simmons M, Tashkin DP. Histopathologic and molecular alterations in bronchial epithelium in habitual smokers of marijuana, cocaine, and/or tobacco. J Natl Cancer Inst. 1998 Aug 19; 90(16): 1198-205. Bifulco M, Laezza C, Portella G, Vitale M, Orlando P, De Petrocellis L, Di Marzo V. Control by the endogenous cannabinoid system of ras oncogene-dependent tumor growth. FASEB J. 2001 Dec; 15(14): 2745-7. Bifulco M, Laezza C, Valenti M, Ligresti A, Portella G, DI Marzo V. A new strategy to block tumor growth by inhibiting endocannabinoid inactivation. FASEB J. 2004 Oct; 18(13): 1606-8. Blazquez C, Casanova ML, Planas A, Del Pulgar TG, Villanueva C, Fernandez-Acenero MJ, Aragones J, Huffman JW, Jorcano JL, Guzman M. Inhibition of tumor angiogenesis by cannabinoids. FASEB J. 2003 Mar; 17(3): 529-31. Blazquez C, Gonzalez-Feria L, Alvarez L, Haro A, Casanova ML, Guzman M. Cannabinoids inhibit the vascular endothelial growth factor pathway in gliomas. Cancer Res. 2004 Aug 15; 64(16): 5617-23. Breuer RH, Pasic A, Smit EF, van Vliet E, Vonk Noordegraaf A, Risse EJ, Postmus PE, Sutedja TG. The natural course of preneoplastic lesions in bronchial epithelium. Clin Cancer Res. 2005 Jan 15;11(2 Pt 1): 537-43. Casanova ML, Blazquez C, Martinez-Palacio J, Villanueva C, Fernandez-Acenero MJ, Huffman JW, Jorcano JL, Guzman M. Inhibition of skin tumor growth and angiogenesis in vivo by activation of cannabinoid receptors. J Clin Invest. 2003 Jan; 111(1): 43-50. Chacko JA, Heiner JG, Siu W, Macy M, Terris MK. Association between marijuana use and transitional cell carcinoma. Urology. 2006 Jan; 67(1): 100-4. Chan PC, Sills RC, Braun AG, Haseman JK, Bucher JR. Toxicity and Carcinogenicity of D9-Tetrahydrocannabinol in Fischer Rats and B6C3F1 Mice. Fundamental & Applied Toxicology 1996; 30: 109–117 Article No. 0048 Ciolino HP, Wang TT, Yeh GC. Diosmin and diosmetin are agonists of the aryl hydrocarbon receptor that differentially affect cytochrome P450 1A1 activity. Cancer Res. 1998 Jul 1;58(13):2754-60. Conney AH. Enzyme induction and dietary chemicals as approaches to cancer chemoprevention: the Seventh DeWitt S. Goodman Lecture. Cancer Res. 2003 Nov 1;63 (21): 7005-31. Contassot E, Tenan M, Schnuriger V, Pelte MF, Dietrich PY. Arachidonyl ethanolamide induces apoptosis of uterine cervix cancer cells via aberrantly expressed vanilloid receptor-1. Gynecol Oncol. 2004 Apr; 93(1): 182-8. Contassot E, Wilmotte R, Tenan M, Belkouch MC, Schnuriger V, de Tribolet N, Burkhardt K, Dietrich PY. Arachidonylethanolamide induces apoptosis of human glioma cells through vanilloid receptor-1. J Neuropathol Exp Neurol. 2004 Sep; 63(9): 956-63. Cottrell JC, Sohn SS, Vogel WH. Toxic effects of marihuana tar on mouse skin. Arch Environ Health. 1973 May; 26(5): 277-8. Duntsch C, Divi MK, Jones T, Zhou Q, Krishnamurthy M, Boehm P, Wood G, Sills A, Ii BM. Safety and efficacy of a novel cannabinoid chemotherapeutic, KM-233, for the treatment of high-grade glioma. J Neurooncol. 2005 Nov 29: 1-10 Efird JT, Friedman GD, Sidney S, Klatsky A, Habel LA, Udaltsova NV, Van den Eeden S, Nelson LM. The risk for malignant primary adult-onset glioma in a large, multiethnic, managed-care cohort: cigarette smoking and other lifestyle behaviors. J NeuroOncol. 2004 May; 68(1): 57-69. Ford D, Vu H, Hauer C, Helzlsouer K, Anthony J. Marijuana Use is not Associated With Head, Neck or Lung Cancer in Adults Younger Than 55 Years: Results of a Case Cohort Study. In: National Institue on Drug Abuse Workshop on Clinical Consequences of Marijuana; August 13, 2001; Rockville, Md. Gallily R, Even-Chena T, Katzavian G, Lehmann D, Dagan A, Mechoulam R. Gamma-irradiation enhances apoptosis induced by cannabidiol, a non-psychotropic cannabinoid, in cultured HL-60 myeloblastic leukemia cells. Leuk Lymphoma. 2003 Oct; 44(10): 1767-73. Gardner B, Zhu LX, Sharma S, Tashkin DP, Dubinett SM. Methanandamide increases COX-2 expression and tumor growth in murine lung cancer. FASEB J. 2003 Nov; 17(14): 2157-9. Green LG, Stein JL, Stein GS. A decreased influence of cannabinoids on macromolecular biosynthesis and cell proliferation in human cells which metabolize polycyclic hydrocarbon carcinogens. Anticancer Res. 1983 May-Jun; 3(3): 211-7. Grimaldi C, Pisanti S, Laezza C, Malfitano AM, Santoro A, Vitale M, Caruso MG, Notarnicola M, Iacuzzo I, Portella G, Di Marzo V, Bifulco M. Anandamide inhibits adhesion and migration of breast cancer cells. Exp Cell Res. 2006 Feb 15; 312(4): 363-73. Hart S, Fischer OM, Ullrich A. Cannabinoids induce cancer cell proliferation via tumor necrosis factor alpha-converting enzyme (TACE/ADAM17)-mediated transactivation of the epidermal growth factor receptor. Cancer Res. 2004 Mar 15; 64(6): 1943-50. Holly EA, Lele C, Bracci PM, McGrath MS. Case-control study of non-Hodgkin's lymphoma among women and heterosexual men in the San Francisco Bay Area, California. Am J Epidemiol. 1999 Aug 15; 150(4): 375-89. Holt VL, Cushing-Haugen KL, Daling JR. Risk of functional ovarian cyst: effects of smoking and marijuana use according to body mass index. Am J Epidemiol. 2005 Mar 15;161(6): 520-5. Hsairi M, Achour N, Zouari B, Ben Romdhane H, Achour A, Maalej M, Nacef T. Etiologic factors in primary bronchial carcinoma in Tunisia. Tunis Med. 1993 May; 71(5): 265-8. Joseph J, Niggemann B, Zaenker KS, Entschladen F. Anandamide is an endogenous inhibitor for the migration of tumor cells and T lymphocytes. Cancer Immunol Immunother. 2004 Aug; 53(8): 723-8. Kaplan NC. Dichloroethyl carbamoyl ester of delta-9-tetrahydrocannabinol. Chemical synthesis and biological testing and evaluation as a potentially site-specific anti-tumor agent. Sci Sin [B]. 1984 Oct;27(10):1048-58. Kogan NM, Rabinowitz R, Levi P, Gibson D, Sandor P, Schlesinger M, Mechoulam R. Synthesis and antitumor activity of quinonoid derivatives of cannabinoids. J Med Chem. 2004 Jul 15; 47(15): 3800-6. Lee SY, Oh SM, Lee SK, Chung KH. Antiestrogenic effects of marijuana smoke condensate and cannabinoid compounds. Arch Pharm Res. 2005 Dec; 28(12): 1365-75. Llewellyn CD, Johnson NW, Warnakulasuriya KA. Risk factors for oral cancer in newly diagnosed patients aged 45 years and younger: a case-control study in Southern England. J Oral Pathol Med. 2004 Oct; 33(9): 525-32. Llewellyn CD, Linklater K, Bell J, Johnson NW, Warnakulasuriya S. An analysis of risk factors for oral cancer in young people: a case-control study. Oral Oncol. 2004 Mar;40(3): 304-13. Massi P, Vaccani A, Ceruti S, Colombo A, Abbracchio MP, Parolaro D. Antitumor effects of cannabidiol, a nonpsychoactive cannabinoid, on human glioma cell lines. J Pharmacol Exp Ther. 2004 Mar; 308(3): 838-45. McKallip RJ, Lombard C, Fisher M, Martin BR, Ryu S, Grant S, Nagarkatti PS, Nagarkatti M. Targeting CB2 cannabinoid receptors as a novel therapy to treat malignant lymphoblastic disease. Blood. 2002 Jul 15;100(2):627-34. McKallip RJ, Nagarkatti M, Nagarkatti PS. Delta-9-tetrahydrocannabinol enhances breast cancer growth and metastasis by suppression of the antitumor immune response. J Immunol. 2005 Mar 15;174(6):3281-9. Montour JL, Dutz W, Harris LS. Modification of radiation carcinogenesis by marihuana. Cancer. 1981 Mar 15;47(6):1279-85. Morgenstern H, Tashkin D, Greenland S, Zhang Z, Cozen W, Mack T. Marijuana use and cancers of the lung and upper aerodigestive tract: results of a case-control study. Presentation at the ICRS Conference on Cannabinoids, 24-27 June, 2005, Clearwater, USA Moscicki AB, Hills N, Shiboski S, Powell K, Jay N, Hanson E, Miller S, Clayton L, Farhat S, Broering J, Darragh T, Palefsky J. Risks for incident human papillomavirus infection and low-grade squamous intraepithelial lesion development in young females. JAMA. 2001 Jun 20;285(23):2995-3002. Munson AE, Harris LS, Friedman MA, Dewey WL, Carchman RA. Antineoplastic activity of cannabinoids. J Natl Cancer Inst. 1975 Sep;55(3):597-602. Murthy NV, Vassell M, Melville GN, Wray SR, Shah D, Wynter HH, West M. Long-term effects of marihuana smoke on uterine contractility and tumour development in rats. West Indian Med J. 1985 Dec;34(4):244-7. Nebert DW, Dalton TP, Okey AB, Gonzalez FJ. Role of aryl hydrocarbon receptor-mediated induction of the CYP1 enzymes in environmental toxicity and cancer. J Biol Chem. 2004 Jun 4;279(23):23847-50. Patsos HA, Hicks DJ, Dobson RR, Greenhough A, Woodman N, Lane JD, Williams AC, Paraskeva C. The endogenous cannabinoid, anandamide, induces cell death in colorectal carcinoma cells: a possible role for cyclooxygenase-2. Gut. 2005 Dec;54(12):1741-50. Portella G, Laezza C, Laccetti P, De Petrocellis L, Di Marzo V, Bifulco M. Inhibitory effects of cannabinoid CB1 receptor stimulation on tumor growth and metastatic spreading: actions on signals involved in angiogenesis and metastasis. FASEB J. 2003 Sep;17(12):1771-3. Recht LD, Salmonsen R, Rosetti R, Jang T, Pipia G, Kubiatowski T, Karim P, Ross AH, Zurier R, Litofsky NS, Burstein S. Antitumor effects of ajulemic acid (CT3), a synthetic non-psychoactive cannabinoid. Biochem Pharmacol. 2001 Sep 15;62(6):755-63. Rosenblatt KA, Daling JR, Chen C, Sherman KJ, Schwartz SM. Marijuana use and risk of oral squamous cell carcinoma. Cancer Res. 2004 Jun 1;64(11):4049-54. Roth MD, Marques-Magallanes JA, Yuan M, Sun W, Tashkin DP, Hankinson O. Induction and regulation of the carcinogen-metabolizing enzyme CYP1A1 by marijuana smoke and delta (9)-tetrahydrocannabinol. Am J Respir Cell Mol Biol. 2001 Mar;24(3): 339-44. Sanchez C, de Ceballos ML, del Pulgar TG, Rueda D, Corbacho C, Velasco G, Galve-Roperh I, Huffman JW, Ramon y Cajal S, Guzman M. Inhibition of glioma growth in vivo by selective activation of the CB(2) cannabinoid receptor. Cancer Res. 2001 Aug 1;61(15):5784-9. Sarfaraz S, Afaq F, Adhami VM, Mukhtar H. Cannabinoid receptor as a novel target for the treatment of prostate cancer. Cancer Res. 2005 Mar 1;65(5):1635-41. Sasco AJ, Merrill RM, Dari I, Benhaim-Luzon V, Carriot F, Cann CI, Bartal M. A case-control study of lung cancer in Casablanca, Morocco. Cancer Causes Control. 2002 Sep;13(7):609-16. Schäfer J, Strimmer K. An empirical Bayes approach to inferring large-scale gene association networks. Bioinformatics. 2005 Mar; 21(6): 754-64. Sheweita SA. Narcotic drugs change the expression of cytochrome P450 2E1 and 2C6 and other activities of carcinogen-metabolizing enzymes in the liver of male mice. Toxicology. 2003 Sep 30; 191 (2-3): 133-42. Sidney S, Quesenberry CP Jr, Friedman GD, Tekawa IS. Marijuana use and cancer incidence (California, United States). Cancer Causes Control. 1997 Sep;8(5):722-8. Talaska G, Schamer M, Bailey JR, Ali SF, Scallet AC, Slikker W Jr, Paule MG. No increase in carcinogen-DNA adducts in the lungs of monkeys exposed chronically to marijuana smoke. Toxicol Lett. 1992 Dec;63(3):321-32. Trivers KF, Mertens AC, Ross JA, Steinbuch M, Olshan AF, Robison LL. Parental marijuana use and risk of childhood acute myeloid leukaemia: a report from the Children's Cancer Group (United States and Canada). Paediatr Perinat Epidemiol. 2006 Mar;20(2):110-8. Uno S, Dalton TP, Derkenne S, Curran CP, Miller ML, Shertzer HG, Nebert DW. Oral exposure to benzo[a]pyrene in the mouse: detoxication by inducible cytochrome P450 is more important than metabolic activation. Mol Pharmacol. 2004 May;65(5): 1225-37. Wang Y, Zhang Z, Yan Y, Lemon WJ, LaRegina M, Morrison C, Lubet R, You M. A chemically induced model for squamous cell carcinoma of the lung in mice: histopathology and strain susceptibility. Cancer Res. 2004 Mar 1;64(5):1647-54. Watson ES. The effect of marijuana smoke exposure on murine sarcoma 180 survival in Fisher rats. Immunopharmacol Immunotoxicol. 1989;11(2-3):211-22. Winterhalder RC, Hirsch FR, Kotantoulas GK, Franklin WA, Bunn PA Jr. Chemoprevention of lung cancer  from biology to clinical reality. Ann Oncol. 2004 Feb;15(2):185-96. Zhang ZF, Morgenstern H, Spitz MR, Tashkin DP, Yu GP, Marshall JR, Hsu TC, Schantz SP. Marijuana use and increased risk of squamous cell carcinoma of the head and neck. Cancer Epidemiol Biomarkers Prev. 1999 Dec;8(12):1071-8. Zhu K, Levine RS, Brann EA, Gu Y, Caplan LS, Hall I, Baum MK. Risk factors for non-Hodgkin's lymphoma according to family history of haematolymphoproliferative malignancies. Int J Epidemiol. 2001 Aug;30(4):818-24. Zhu K, Levine RS, Brann EA, Hall HI, Caplan LS, Gnepp DR. Case-control study evaluating the homogeneity and heterogeneity of risk factors between sinonasal and nasopharyngeal cancers. Int J Cancer. 2002 May 1;99(1):119-23. Zhu LX, Sharma S, Stolina M, Gardner B, Roth MD, Tashkin DP, Dubinett SM. Delta-9-tetrahydrocannabinol inhibits antitumor immunity by a CB2 receptor-mediated, cytokine-dependent pathway. J Immunol. 2000 Jul 1; 165(1): 373-80.
  • There is an element of truth in this statement, but one must also look at it from a larger perspective. Yes, smoking marijuana or hashish is somewhat worse that smoking a tobacco cigarette. Inhaling the smoke from any kind of burning vegetation irritates the lining of your lungs. Many of the chemical by-products of combustion are unhealthy and some are known carcinogens. You are also likely to be inhaling burning pesticide residues. The smoke from many commonly inhaled products, such as tobacco, marijuana, sweetgrass, and incense, are all bad for your lungs. However, the effects of these products are directly linked to the amount you smoke. A heavy smoker may smoke 50 cigarettes a day, far worse for your health than smoking one cigarette a day - or one joint. Most of the commonly inhaled products are inhaled without any filtration. The filters on cigarettes do not eliminate the dangers of tobacco smoke, but they do reduce the amount of tar and resins inhaled into your lungs. In general, plain cigarettes do more damage to your lungs than filter-tipped cigarettes. I have yet to see a commercially-produced joint with a filter. In that sense, smoking a joint may cause more harm to your lungs than smoking a cigarette. Again, there is that small matter of scale: cigarette smokers commonly smoke 20 cigarettes a day, but not many marijuana users smoke anything approaching that number. Marijuana smokers tend to inhale and hold their breath for a longer period of time than do tobacco smokers. This gives the active ingedients of the drug more time to transfer into the smoker's bloodstream. It also provides a longer period of time for the smoke to cool. This allows a higher percentage of the constituents of the smoke to adhere to the lining of the lungs. This also makes smoking marijuana somewhat less healthy than smoking a tobacco cigarette. But again, there is that matter of scale. If you are concerned about the effects of marijuana smoke, then I would suggest you get a little creative with your baking. Cooking your marijuana, hashish, or hash oil into a batch of chocolate brownies may not be as effective a method of getting THC into your bloodstream, but it does eliminate any concerns over the health effects of smoking such products. And if you suffer from asthma, this is a good way to get a little high without the smoke triggering an attack. Like I said at the beginning, it is all a matter of scale. If you like to spend your Friday evenings smoking a couple of joints, I would not overly worry about the damage to your lungs.
  • It is assumed that marijuana smokers use no filters.
  • isn't a joint equal to 4 or more cigarettes
  • Okay a ton of people have told me that it is but there is always the alternative to smoking a joint...the bong. The water bong filters 80% of the smoke and leaves mostly just THC. Much better don't you think?
  • No... it is an all natural herb, tabacco is not and can contain upto 200 differant carcinogens compared to about 60 in marijuana. The whole deal about anti-marijuana campaigns is to brainwash the public about the benefits of hemp as a cash crop, the sum of which would alter the stock market considerably and screw up the economy big time. In other words marijuana could become a type of underground currency. It's impact as a cash crop would send the world economies reeling and make money and credit obsolete. The WTO doesnt ever want that to happen because then they would all be out of a job, so they came up with some anti-science and paid the campaigns of numerous politicians to make it an illegal substance for you to have.... they did the same thing with gold everyone knows that.
  • This myth was brought on by Dr. Tashkin's original research, the study cited by the ONDCP - who made the claim of marijuana being more harmful than one Pack (or 16, or maybe just 4) Cigarettes. Anyone notice that recently the ONDCP (your tax $) advertisements have gotten really lame? Watch one- http://www.answerbag.com/a_view/989954 Why are they so lame now? ¤ Donald Tashkin led a team of UCLA investigators who conducted a new study: "We did not observe a positive association of marijuana use, even heavy long-term use, with lung cancer, controlling for tobacco smoking and other potential confounders" (age, sex, race, educational level). "Study Finds No Cancer-Marijuana Connection" http://www.washingtonpost.com/wp-dyn/content/article/2006/05/25/AR2006052501729_pf.html Dr. Donald Tashkin federal Government researcher from UCLA School of Medicine:
  • This is a very difficult topic for me and I am trying to research it to get answers. I have smoked pot myself on and off since I was a teenager. My significant other smokes it on a daily basis, much like a cigarette. I recently graduated and now am a respiratory therapist. I understand the effect that it has on the lungs. I think that the reason it is hard to say is because most pot smokers also smoke cigarettes. My sig other only smokes pot. I would love to open him up and look at his lungs when he dies. I GAURANTEE without a doubt that he will get some form of lung disease or disorder just like those who smoke cigarettes. He believes in the medical use however it is true THC can help but when it is smoked and inhaled it can be very harmful to your body. I think that just as we have different ways to administer drugs....THC could probably be very helpful but how it is administered is the big issue. I to believe that this is the way people are trying to get it legalized is by showing a medical way of helping. Name one drug that is smoked and approved by the FDA....you won't find one because smoking anything is not good for your lungs and body. I know they have THC in form of a pill but does that really work. How can a person make THC in pill form and have it work like it would in its natural form? I am stuck in the middle and can't seem to find any real proof other than books I have studied but because of the complexity of the issues no one can really proove anything.......UGGHHHHH..
  • no it is not---unless you do not know what pesticides were used and how they smuggled it inside the usa...sometimes that matters...reefer is good for you...
  • A joint is unfiltered, but then again pot doesn't include all the chemicals that cigs do.
  • It has fewer chemicals than cigarettes, but the human lungs weren't meant to inhale smoke like that, so it still is bad for your lungs and i don't recommend it at all.
  • Yes, the whole reason you can see smoke is because it is made up of tiny particles, and when you draw them into your lungs, they clog up the air pockets. Chronic Obstructive Lung Disease is very high among marijuana smokers, rather than the lung cancer from carcinomas you find in cigarettes.
  • Any smoke is bad for the lungs with no exception for Marijuana
  • yeah I hear marijuana is worst then ciggs. :( Then again I guess it depends on how much you smoke. A joint every now and then won't be as bad as a half pack of ciggs a day. But if you are smoking weed every day, it is probably pretty bad for you.
  • You shouldn't smoke your pot...you should ingest it. Better for you. But that being said, marijuana does not have all of the chemicals in it to keep it fresh like cigs do. Plus, people typically smoke less pot than they would cigs. So I would think it would be less harmful. But I would have to see some documented proof to know for sure.
  • It honestly depends on how much pot you are talking about in comparison to however many cigarettes. Smoking a bowl a day is much less harmful than smoking a pack of cigarettes a day, but when you compare smoking an equal amount of each material, I'd say that cigarettes are less harmful. Most people who smoke pot don't smoke as much material on a daily basis as most people who smoke cigarettes. I think that the pot smoker has healthier lungs more often than the cigarette smoker, but the method of smoking does have a better or worse effect on the lungs. Smoking both pot and cigarettes is asking for trouble down the road, unless you are very moderate about it. A vaporizer is the greatest way of smoking pot, by far. I would like to say that it is totally harmless but I don't know for sure if that is a fact. A vaporizer is what my doctor recommended to me, and a bong was recommended as a second best method of inhaling the material.
  • cigarettes contain carbon monoxide which is very harmfull for the lungs and body
  • yes smoking buddz is worst fer yur lungs cuz of awl dhat rezzin a joint iz lyk a pack of quarez or a bleezy/blunt iz lyk cigarz buht buddz iz lyk dha shyt niggah! -j-skizzie

Copyright 2023, Wired Ivy, LLC

Answerbag | Terms of Service | Privacy Policy