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Comparative Toxicology of Cigarette Smoke and Automobile ExhaustBY: Sonali Bhawsar | Category: Toxicology | Submitted: 2011-03-01 05:46:59
Comparative toxicology of cigarette smoke and automobile exhaust It is hard to believe that cigarette and automobile have comparable characteristics. The worst thing what I found while searching for hazardous companion for cigarette was that there is nothing as hazardous as cigarette smoke (CS). CS contains approximately 5000 chemical compounds and at least 90 of them are known carcinogens. Automobile exhaust (AE) was chosen from a big list of dangerous chemicals contained in pesticides, industrial effluents or spent wash; in which maximum number of comparable parameters are present. Both CS and AE are indoor and outdoor pollutants. CS is complex mixture of ethylene oxide, acrylonitrile, benzene, acetaldehyde, arsenic compounds, ammonia, formaldehyde, beryllium, furan, sulfur compounds, nitrogen oxides, isoprene, hydrazine, lead, nitromethane, carbon monoxide, polonium, tar, toluidine, vinyl chloride, N-nitroso derivatives like nitrosoorcinicotine and 50 different polyaromatic hydrocarbons (PAHs). You must be known that cigarette is made up of ground tobacco (Nicotiana tabacum) leaves. Nicotine is active principle component of tobacco; a cigarette contains 10mg of nicotine. Chemically, nicotine is an alkaloid and also used as pesticide. When cigarette is lit, nicotine reaches brain in less than 7 seconds and 1mg is delivered into the smoker's body via blood. Vomiting, sweating, palpitation, seizures, stomach cramps, acidity, drooling, pallor and nausea are some of the common signs of nicotine poisoning found in non-smokers including children. Similar symptoms are also observed in farmers using nicotine as pesticide and tobacco harvesters. In smokers, toxic effects like diarrohea, salivation, vomiting, nausea, mental confusion, impairment sense of taste and smell, weakness and dizziness are observed on acute exposure. Fatal toxicity is indicated by decreased blood pressure, irregular pulse, breathing difficulty, convulsions, lack of concentration, polycythemia, respiratory failure and death. Smoking habit in pregnant women results in fatal fetal toxicity such as decreased birth weight and attention deficit disorder. Nicotine withdrawal symptoms are also very nauseating like impatient and restless behavior, irritability, weight gain and chronic depression. Smokeless tobacco causes nonfunctional reproductive system, Raynaud's syndrome, heart disease, mouth ulcers, gum disease and nicotine addiction. Thus nicotine in CS is potent carcinogen and adverse psychostimulant. It is more toxic than cocaine; toxicity analysis in experimental rats showed that LD50 of nicotine was 50mg while that of cocaine was only 5mg/kg. AE is generated by combustion of fuels such as diesel, petrol, coal, natural gas or kerosene used in automobiles. It is discharged into the atmosphere via exhaust pipe of automobile. Typically, an AE contains carbon dioxide, carbon, monoxide, nitrogen, nitrogen oxides, ammonia, hydrogen, formaldehyde, hydrocarbons and PAHs, sulfur, sulfur oxides, lead derivatives, tar, ozone, unused oxygen, water vapor and particulate matter in the form of soot. These constituents are hazardous to health of plants, animals and human beings and also to environment. Formation of photochemical smog, plant damage, acid rain, pulmonary irritation, eye irritation, anemia, odema and lung cancer are some of the toxic effects of AE. The effect of 3 common constituents, formaldehyde, carbon monoxide and PAHs in CS and AE is reviewed in following paragraph. Formaldehyde is carcinogenic chemical. Inhalation of vapors causes watery eyes, burning sensation in throat, irritation of nasal membrane, difficulty in breathing, and it is known to aggravate the symptoms of asthma. Carbon monoxide (CO) is tasteless, odorless, colorless, nonirritating, difficult to detect and hence a silent killer gas. CS and AE contain nearly 5% and 1% CO respectively; in CS, sometimes greater than 5%. CO combines with hemoglobin in blood forming very stable carboxyhemoglobin resulting in diminished oxygen supply, polycythemia and rapid blood clot. Approximately 30 minutes of exposure to CO is considered lethal to generate toxic effects like vertigo, sequelae, hypoxia, memory loss, depression, central nervous system and heart dysfunction and death. PAHs are apparently useless chemicals generated during incomplete combustion. They can be found in any environment like soil, water, air or human body. They don't dissolve in water and hence are persistent recalcitrant compounds. PAHs such as pyrene, fluorene, chrystene, benzofluoranthene, naphthalene and acenaphthalene are the constituents of CS and AE. Their health hazards include asthma, heart attack, pulmonary diseases and odema. Severity of toxicity is dependent upon dose, exposure time and route of entry. To summarize, both CS and AE increase the chances of developing Alzheimer's and Parkinson's disease, CS is 10 times more potent air pollutant than AE, CS is 50 times more responsible for heart disease and lung cancer and the risk of illness and death resulting from CS is more than AE. Simply to mention, unlike smoking, AE is not a habit hard to quit but a manmade source of pollution; therefore easy to monitor and control. Article Source: http://www.biotecharticles.com/ About Author / Additional Info: Comments on this article: (2 comments so far)
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