Cigarette smoking, risk

A final area of research focuses on how the piU. can best be used by women. Physicians used to recommend pid-free hoHdays, but it is now known that there is no vaUd reason for this practice. Similarly, further research indicated that the U.S. EDA s restrictive guidelines for prescribing the piU. to women over the age of 35 are not justified, and those guidelines have been changed. EinaHy it is clear that cigarette smoking increases the risk of cardiovascular side effects, especially in women over 35 who utilize combination oral contraceptives. 

A problem exists in the perception of risk because the experts and lay people s views differ. The experts usually base their assessment on mortality rates, while the lay people s fears are based on "outrage" factors. In order to help solve tliis problem, in tlie future, risk nimuigcrs must work to make truly serious hazards more outrageous. One example is tlie ongoing concern for tlie risk involved in cigarette smoke. Another effort must be made to decrease tlie public s concern with low to modest hazards, i.e., risk managers must diminish "outrage" in these areas. In addition, people must be treated fairly and honestly. 

A susceptible population will exhibit a different or enhanced response to methyl parathion than will most persons exposed to the same level of methyl parathion in the environment. Reasons may include genetic makeup, age, health and nutritional status, and exposure to other toxic substances (e g., cigarette smoke). These parameters result in reduced detoxification or excretion of methyl parathion, or compromised fimction of organs affected by methyl parathion. Populations who are at greater risk due to their imusually high exposure to methyl parathion are discussed in Section 6.7 Populations With Potentially High Exposures. 

The a-tocopherol, P-carotene (ATBC) Cancer Prevention study was a randomised-controlled trial that tested the effects of daily doses of either 50 mg (50 lU) vitamin E (all-racemic a-tocopherol acetate), or 20 mg of P-carotene, or both with that of a placebo, in a population of more than 29,000 male smokers for 5-8 years. No reduction in lung cancer or major coronary events was observed with any of the treatments. What was more startling was the unexpected increases in risk of death from lung cancer and ischemic heart disease with P-carotene supplementation (ATBC Cancer Prevention Study Group, 1994). Increases in the risk of both lung cancer and cardiovascular disease mortality were also observed in the P-carotene and Retinol Efficacy Trial (CARET), which tested the effects of combined treatment with 30 mg/d P-carotene and retinyl pahnitate (25,000 lU/d) in 18,000 men and women with a history of cigarette smoking or occupational exposure to asbestos (Hennekens et al, 1996). 

Factors that predispose an individual to IHD are listed in Table 4—2. Hypertension, diabetes, dyslipidemia, and cigarette smoking are associated with endothelial dysfunction and potentiate atherosclerosis of the coronary arteries. The risk for IHD increases two-fold for every 20 mm Hg increment in systolic blood pressure and up to eight-fold in the presence of diabetes.5,6 Physical inactivity and obesity independently increase the risk for IHD, in addition to predisposing individuals to other cardiovascular risk factors (e.g., hypertension, dyslipidemia, and diabetes). 

COPD includes chronic bronchitis and emphysema. Chronic bronchitis is defined clinically as a chronic productive cough for at least 3 months in each of two consecutive years in a patient in whom other causes have been excluded.1 Emphysema is defined pathologically as the presence of permanent enlargement of the airspaces distal to the terminal bronchioles, accompanied by destruction of their walls without obvious fibrosis.1 The major risk factor for both conditions is cigarette smoking, and many patients share characteristics of each condition. Therefore, new consensus guidelines have moved away from using these subsets and instead focus on chronic airflow limitation. 

In an early study in 1971, Cole22 found an association between coffee drinking and lower urinary tract cancer based on a case-control study of 445 cancer patients (345 men, 100 women) and 451 population controls who were matched for age and sex. The analyses had controlled for cigarette smoking and occupation however, there was no consistent dose response relation, and the summary risks were significant only in women,... 

In an investigation of caffeine-containing products in 1993, Slattery et al.75 reported on alcohol, coffee, tea, caffeine, and theobromine intake and the risk of prostate cancer in a Utah study. Data were gathered from a population-based sample of 362 newly diagnosed cases of prostate cancer and 685 age-matched controls. The Utah population was comprised predominantly of members of the Church of Jesus Christ Latter-Day Saints. The researchers found that pack-years of cigarettes smoked and consumption of alcohol, coffee, tea, and caffeine were not associated with prostate cancer risk, but found some possible correlation with increased theobro-... 

Ross, R. K., Paganini-Hill, A., Landolph, J., Gerkins, V., Henderson, B. E., Analgesics, cigarette smoking, and other risk factors for cancer of the renal pelvis and ureter, Cancer Res, 49, 1045, 1989. 

Haglund B, Cnattingius S. 1990. Cigarette smoking as a risk factor for sudden infant death syndrome A population-based study. Am J Public Health 80 29-32. 

Shields PG et al. Dopamine D4 receptors and the risk of cigarette smoking in... 

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