Tobacco Exposure : The Risk Factors For Coronary Artery Disease

Everyone knows that smoking is a major health hazard: it’s the leading preventable cause of death in the United States. But some people may be surprised to learn that smoking is also the most potent cardiac risk factor, increasing risk by 250 percent. Another surprise: exposure to secondhand smoke is also a major cardiac risk factor, which is why passive smoking is the nation’s thirdleading preventable cause of death. (Alcohol is the second.)
In all, smoking accounts for 20 percent of all deaths from coronary artery disease. But within a year of quitting, smokers can cut this risk in half. Within two years, the cardiovascular risk for a former smoker is very close to that of a person who never smoked. Because smoking probably contributes to blood vessel inflammation, removing that irritant should slow the inflammatory process, resulting in a quick drop in heart disease risk.

I see a lot of patients who know they should quit smoking, but they’re not sure how. The best approach is two-pronged: use medicine, and get counseling and support.
Easing the craving for nicotine is a key part of stopping smoking. Nicotine patches, gum, lozenges, nasal spray, and cigarette-shaped inhalers deliver enough nicotine to satisfy the body without the tar, carbon monoxide, and other harmful chemicals found in cigarette smoke. An antidepressant known as bupropion (Zyban, Wellbutrin) also alleviates the symptoms of nicotine withdrawal, even in people who aren’t depressed. Combining bupropion and nicotine replacement may work the best of all.
Nicotine replacement is safe, even after a heart attack, and it’s much safer than continued smoking. These products don’t increase the clotting potential of blood or damage the fragile but important lining of blood vessels, as smoking does.
Nicotine replacement often isn’t enough on its own. Counseling and social support can help you break your “smoking cues,” the things you link to lighting up, like drinking coffee or finishing a big meal. You can get counseling one-on-one at a support group run by a hospital or local department of health, via the phone, or online. (Some options are listed in the Resources section.)
Remember that quitting smoking is a huge change, so it might take you a few tries to get off cigarettes for good. If you slip by having a cigarette or two after your quit date, try to figure out what went wrong and how to fix it the next time. Don’t convince yourself that as long as you had one, you may as well have another, and another. . . . The same holds true if you return to your old smoking habit. You may have to quit a few times. Not succeeding may just mean you need more help.

Salt Affects Your Blood Pressure

What causes high blood pressure? Medical Science recognizes many causes: tension, strains, stress, toxic substances such as cigarettes and gasoline, food additives, insecticide sprays, etc. and the side effects of drugs and industrial toxins are all suspect. What can you do to protect yourself from these injurious agents? You would do well to exclude as many of these harmful factors from your environment and life as soon as possible!
However, there is one cause of high blood pressure which can be easily avoided. Sodium chloride (common table salt) is the major cause of high blood pressure! Up to now, we have been talking about causing high blood pressure in the normal person. But how about the effects of salt on those millions suffering from our country’s most prevalent and preventable ailment – excess weight? This is a prime area for research because obesity is known to be frequently accompanied by high blood pressure. Medical researchers proclaim a link between high blood pressure and salt intake in obesity.

Smoking Has Many Ways to Kill You!

The body has no defense against carbon monoxide produced by smoking. You have read about people committing suicide or being killed by carbon monoxide fumes. Why deliberately breathe them into your lungs? The coal tars in tobacco are the chief poisons responsible for cancer of the lungs, mouth and related areas of the body. It frightens us to think of what will happen in another 25 years because of the excessive use of tobacco. We are convinced that every smoker will eventually develop lung, throat or some form of cancer –if heart disease or something else doesn’t kill them first!
The results of a recent federal health study found that cigars are no less hazardous than other forms of tobacco, and therefore needs stronger federal regulation! The absence of such warning labels on cigars could lead consumers to erroneously conclude that cigars don’t carry health risks. Beware – there is no safe form of deadly tobacco! Cigars are becoming tremendously popular and sales have jumped 18% recently. Yet cigar smokers and tobacco chewers face grave risk of diseases such as mouth, throat, esophageal, larynx and lung cancer, as well as coronary heart disease and chronic obstructive pulmonary disease. Fact: cigars contain up to 90 times as much of some cancer-causing agents as cigarettes do!

Tobacco – Enemy of Your Heart and Health

Whether it’s cigarettes, cigars or pipes, tobacco is one of the heart’s worst enemies! Here is what Dr. Lester M. Morrison, noted California heart specialist and pioneer in the low-cholesterol diet for the treatment and the prevention of heart disease, said about tobacco:
Tobacco is a poison. Nicotine, the main ingredient of tobacco, is a poison affecting the brain, heart and other vital organs. The tobacco plant is directly related to the deadly nightshade family of plants. Aside from the chief poison, nicotine, there are other well-known poisons present in tobacco: arsenic and coal tar substances and carbon monoxide (when tobacco is burned).
Dr. Morrison also said, Nicotine is the most noxious substance that affects the blood vessels in man. Nicotine is a powerful drug that constricts the arteries, narrowing still more the vital passageways of the blood, already clogged by other toxic residue. The tobacco smoker does double damage to his heart – first, by filling the bloodstream with the harsh poisons of tobacco and, second, by narrowing the arteries and other blood vessels, preventing a free flow of life-giving blood.

Factors behind health behaviours

Behaviours which are generally assumed to be healthy include physical exercise, a moderate intake of alcohol and fat, and dental hygiene, while unhealthy behaviours are, for example, the use of drugs, sweets, alcohol and tobacco, as well as being under lots of psychological stress. British teenagers considered exercise as the main factor good for their health and dieting the main factor which was bad for their health. By dieting they meant socalled “junk food” and sweets especially; smoking was also considered bad. Healthy eating, exercise, and non-smoking were main factors related to health also in other studies conducted in Britain and Finland. Behaviours including tobacco use, a poor diet, physical inactivity and alcohol abuse are actually the biggest cause of death in the USA.
It has been suggested that people’s health behaviour is influenced by both individual attributes and the conditions they live under. Cohen, Scribner and Farley (2000) identified four categories of factors which are assumed to influence health behaviour:

• Availability of products (protective or harmful), referring to accessibility of products associated with health outcomes, such as tobacco or high-fat foods or fruit and vegetables.
• Physical structures which either increase or reduce opportunities for healthy behaviours, such as consumer products, buildings or neighbourhoods. Well-lit streets, for example, reduce opportunities for assault or injury; childproof medicine containers reduce the risk of poisoning for children.
• Social structures and policies: laws or policies which require or prohibit behaviours, such as laws against selling alcohol to underage people.
• Media and cultural messages. Culture and media messages refer to messages that people see or hear often, and which can either increase or decrease consumption − for example, of tobacco, alcohol or high-fat food.

These factors can all complement each other. The accessibility of harmful products can be reduced through social structures and the media can enhance the other structural factors when messages reinforce behaviours which are promoted by the other structural interventions (Cohen, Scribner & Farley 2000).

EFFECTS OF WORK STRESS ON BEHAVIORAL OUTCOMES :Caffeine Ingestion

Caffeine is the most widely consumed pharmacologically active substance in the world. The evidence on its possible implications for human health, that is, whether it has chronic physiological effects on habitual consumers, is as yet inconclusive (Benowitz, 1990). It has long been suspected that repeated exposure to caffeine may produce tolerance to its physiological effects (James, 1994). The consumption of caffeine is known to improve physical performance and endurance during prolonged activity at sub-maximal intensity (Nehling & Debry, 1994). Caffeine’s physiological effects are linked to the antagonism of adenosine receptors and to the increased production of plasma catecholamines (Nehling & Debry, 1994).
The study of the relationship between work-related stress and caffeine ingestion is confounded
by the high correlation between coffee consumption and smoking (Conway et al., 1981). A meta-analysis of six epidemiological studies (Swanson et al., 1994) has shown that about 86% of smokers consumed coffee while only 77% of the non-smokers did so.Three major mechanisms have been suggested to account for this close association between caffeine intake and smoking: (a) conditioning effect, (b) reciprocal interaction; that is, caffeine intake increases arousal while nicotine intake decreases it, and (c) the possibility of a third variable affecting both. Stress, and particularly work-related stress, is a possible third variable influencing both caffeine and nicotine intake (Swanson et al., 1994).
Caffeine consumption is often regarded as reinforcing and augmenting the psychological and physiological effects of stress (France&Ditto, 1992; Lane et al., 1990). This synergetic relationship has been explained as due to the effects of both on the elevation of blood catecholamines (Lane et al., 1990). Experimental laboratory studies have found that as opposed to a placebo drink, consumption of high levels of caffeine interacts with stress in worsening the effects of stress on psychological and physiological strain (France & Ditto, 1992; Lane & Williams, 1987).

EFFECTS OF WORK STRESS ON BEHAVIORAL OUTCOMES :Smoking Behavior

Cigarette smoking and the use of other tobacco products constitutes the single most devastating
preventable cause of death in many market economies (Quick et al., 1997). A large body of epidemiological, clinical and pathological studies relates cigarette smoking to the development of cardiovascular heart disease and other chronic diseases, including emphysema, chronic bronchitis and non-fatal strokes. Moreover, a considerable body of research has demonstrated the adverse health consequences of passive smoking, the involuntary exposure of non-smokers to tobacco smoke from smokers in confined environments. This research has led many countries to regulate smoking in public places (Quick et al., 1997). As is the case with the other behavioral outcomes considered here, smoking behavior is multifactorial in its etiology, and there is zvidence pointing to its genetic origins. Twin studies have demonstrated that genetic factors contribute to the initiation of smoking and influence the intensity of smoking cigarettes (number of cigarettes smoked per day; see Pomerleau & Kordia, 1999). A meta-analysis of the data from five studies, each involving more that 1000 twin pairs, found an estimated 60% of the propensity to smoke may be explained by genetic factors (Heath&Madden, 1995). Cigarette smokers are over-represented in many disadvantaged groups, including those with psychiatric and behavioral disorders (Parrott, 2000). Still, there is evidence that environmental and job-related stress may account for a significant proportion of the variance of smoking behavior. Consequently, interest in the pathway leading from stress, and stress at work, to smoking behavior is growing.
Stress and associated emotional responses, including anxiety and irritability, are attenuated by smoking. These effects have been shown to be short-lived (Parrott, 1995). Mood and affective state impairments tend to occur between cigarettes in a repetitive cycle. This cycle provides a clear rationale for the addictive use of cigarettes (Parrott, 1995). Smokers, therefore, obtain only short relief from adverse states of anxiety and irritability that follow the experience of stress. There is evidence from smoking abstaining studies that nicotinewithdrawal symptoms are worse under high environmental stress than under low environmental stress, while post-cigarette relief was also correspondingly greater (Parrott, 2000).
In empirical research, stress is often found to predict smoking behavior while interacting with other predictors, like lack of social support. In a review of the research on smoking behavior among nurses, Adriaanse et al. (1991) found that excessive smoking among both female and male nurses was explained by work stress, lack of social support, and unmet expectations that characterize nurses’ professional socialization. Nurses’ smoking is considered a public health problem since they often act as role models to patients and their families. In several studies, smokers who express high motivation to smoke have reported above-average stress that they had experienced before the smoking, rather than belowaverage stress after smoking (Parrott, 1995). Consequently, stress management and anxiety reduction programs at the workplace have the potential to influence motivation to smoke. Workplace-based smoking cessation programs do bring to the fore, however, the conflict between health and performance. Among aviators, as an example, smoking is a health hazard in the cockpit. Pilots who are required to abstain from smoking during and before flights may suffer cockpit performance decrements (Sommese & Patterson, 1995).
Yet another facet of the complex relationship between stress and cigarette smoking was described by Parrott (1999), who proposed that the evidence on this relationship might be reinterpreted to suggest that smoking actually causes stress. Parrott (1999) pointed out that regular smokers are more stressed than their non-smoking counterparts and that smokers experience an overall reduction in stress when they quit smoking. Another theory holds that
smoking may redistribute stress by modulating moods (Piasecki & Baker, 2000).
Work organizations contribute to and may inhibit (or induce) smoking behavior by three basic processes documented in the research literature. First, work organizations may develop organizational norms with respect to smoking on the job, including the local official definition of permissible smoking and the mechanisms of its control established by management. Second, stressful working conditions, like sustained overload or machine-paced jobs characterized by lack of control, may induce heavy smoking as a coping strategy to alleviate the stressful job conditions. Third, work organizations may explicitly or implicitly encourage the development of occupationally based smoking subcultures. In a survey of 12 000 professional people in 14 occupational categories, Russek (1965) found significant differences in the prevalence of smoking in high-stress occupations as compared with low-stress occupations.