Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0242379 (lung cancer)
 71,905 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In 1992, the U.S. Environmental Protection Agency (EPA) issued a "draft" assessment of ETS and lung cancer in adults and respiratory disorders in children. Relying on weak and inconclusive epidemiological data, the supposed similarity between ETS and MS, the presence of "known or suspected carcinogens" in MS and by extrapolation in ETS, and the "biological plausibility" of an adverse relationship between ETS and health, the EPA recommended that ETS be classified as a "Group A (known human) carcinogen." Fundamental physical and quantitative chemical differences among ETS, MS, and SS and human exposure to each smoke were disregarded: The three are not equivalent nor is ETS exposure a quantitative variant of cigarette smoking. A substantial difference in retention percentage overlays the huge dosimetric difference between exposures. As a result, the "dosage" of ETS retained is miniscule relative to MS. Also, conclusions reached by the EPA and the use of tenuous relationships as bases for Group A classification are unwarranted because of failure to consider the data upon which the "tumorigenicity" of the ETS components was based, questions on the presence and/or levels of these components in MS, and data indicating that a 25- to 30-fold decrease of a high-level dose of MS or MS condensate diminished the effects observed in bioassays from pronounced to zero, i.e., a threshold was demonstrated. Finally, EPA overlooked the more than 100 tobacco smoke components known to inhibit the tumorigenic action of many of the listed "tumorigens."
 ...
PMID:Environmental tobacco smoke. 129 40

This paper demonstrates that Wald's meta-analysis is an unadjusted combination of unadjusted estimates. There are many differences among the design and implementation of the original studies combined here. One consequence of these differences is that studies of spousal smoking and lung cancer mortality conducted in the United States have a lower combined RR than those done elsewhere. Here it is shown that adjustment for this stratification results is a non significant finding as to the association of ETS with lung cancer. Likewise, the addition, for illustration, of Varela's Ph.D. thesis that is the largest case-control study to date, changes the overall results from a significant to a non-significant result. This paper does not attempt to update Wald's meta-analysis with more recent studies. This is being done, I believe by the Environmental Protection Agency. I have given here my reasons for suspecting the conclusions of meta-analysis of non-randomized studies and the illustrations provided here of the effect of publication bias and covariate adjustment support this view.
 ...
PMID:The epidemiology of environmental tobacco smoke (ETS) and the weight of evidence argument. 138 92

Adequate information is available linking ETS to several medical problems, including respiratory illnesses in children and lung cancer in adults; nonetheless, continuing investigation is necessary to clarify several issues. Reliable information needs to be gathered on the quantity and fate of ETS chemicals in ordinary indoor environments; improved surveys quantifying passive smoke exposure should be tested along with the use of biologic markers to quantify exposure-dose relationships in nonsmokers. To date, legislation and private initiatives have been the most promising of the various measures to protect nonsmokers from ETS. While nonsmokers' judicial action has had variable success, it places the burden of challenging smoking on the nonsmoker, and it entails piecemeal, case-by-case resolution. On the other hand, legislation and private policies relieve the nonsmokers' burden to initiate the challenge, and they protect greater numbers of nonsmokers. Furthermore, legislation and policies may have a great number of direct and indirect effects. In the short term, legislation and policies that are adequately implemented and enforced alter the behavior of smokers in areas where smoking is prohibited and should result in a reduced concentration of tobacco smoke in those areas. In the long term, policies and legislation that restrict smoking in public places and the workplace help to reinforce nonsmoking as the normative behavior in society. Smoking restrictions increase public awareness and acceptance of health risks of tobacco smoke. The combination of altered social norms and reduced opportunities to smoke may encourage smokers to quit and nonsmokers, especially adolescents, not to start.
 ...
PMID:Environmental tobacco smoke. Medical and legal issues. 154 67

The evidence that ETS increases risk of death from heart disease is similar to that which existed in 1986 when the US Surgeon General concluded that ETS caused lung cancer in healthy nonsmokers. There are 10 epidemiological studies, conducted in a variety of locations, that reflect about a 30% increase in risk of death from ischemic heart disease or myocardial infarction among nonsmokers living with smokers. The larger studies also demonstrate a significant dose-response effect, with greater exposure to ETS associated with greater risk of death from heart disease. These epidemiological studies are complemented by a variety of physiological and biochemical data that show that ETS adversely affects platelet function and damages arterial endothelium in a way that increases the risk of heart disease. Moreover, ETS, in realistic exposures, also exerts significant adverse effects on exercise capability of both healthy people and those with heart disease by reducing the body's ability to deliver and utilize oxygen. In animal experiments, ETS also depresses cellular respiration at the level of mitochondria. The polycyclic aromatic hydrocarbons in ETS also accelerate, and may initiate, the development of atherosclerotic plaque. Of note, the cardiovascular effects of ETS appear to be different in nonsmokers and smokers. Nonsmokers appear to be more sensitive to ETS than do smokers, perhaps because some of the affected physiological systems are sensitive to low doses of the compounds in ETS, then saturate, and also perhaps because of physiological adaptions smokers undergo as a result of long-term exposure to the toxins in cigarette smoke. In any event, these findings indicate that, for cardiovascular disease, it is incorrect to compute "cigarette equivalents" for passive exposure to ETS and then to extrapolate the effects of this exposure on nonsmokers from the effects of direct smoking on smokers. These results suggest that heart disease is an important consequence of exposure to ETS. The combination of epidemiological studies with demonstration of physiological changes with exposure to ETS, together with biochemical evidence that elements of ETS have significant adverse effects on the cardiovascular system, leads to the conclusion that ETS causes heart disease. This increase in risk translates into about 10 times as many deaths from ETS-induced heart disease as lung cancer; these deaths contribute greatly to the estimated 53,000 deaths annually from passive smoking. This toll makes passive smoking the third leading preventable cause of death in the United States today, behind active smoking and alcohol.
 ...
PMID:Passive smoking and heart disease. Epidemiology, physiology, and biochemistry. 191 25

Cigarette smoking remains the primary cause of preventable death and morbidity in the United States. Smoking causes lung cancer, COPD, and CHD and contributes significantly to mortality from other conditions such as stroke. Maternal smoking during pregnancy causes low birthweight and perinatal mortality, and it may have lasting impact on the child's physical and cognitive growth. Passive exposure to ETS causes lung cancer and poses particular danger to the respiratory health of young children. Smoking cessation strategies are important, but the should be supplemented by community and policy-level interventions. Workplace or community smoking bans, statewide taxes on tobacco, and antismoking media campaigns may be effective adjuncts to individual cessation strategies. These strategies may be an even more important disincentive to smoking initiation. The expanding horizon of health consequences of smoking and its costs to American society should again challenge public health agencies to develop and implement effective strategies to prevent smoking acquisition by young people. These health effects should also motivate health professionals in other countries where smoking prevalence is increasing, rather than decreasing, to initiate more effective efforts to reverse this trend and minimize the excess morbidity and death that accompany this dangerous habit.
 ...
PMID:Cigarette smoking and health. American Thoracic Society. 856 46

The association between exposure to ETS and the risk of lung cancer in life-time non-smoking women was investigated by means of a hospital based case-control study in Moscow, Russia. The main importance of our study is that it was conducted on a population with a specific smoking pattern from which no information is available on health effects of ETS. A total of 189 incident cases of histologically confirmed lung cancer were identified in 2 principal cancer treatment hospitals in Moscow. A total of 358 female oncology patients from the same hospitals were selected as controls. The controls matched by the hospitals to the cases were similarly restricted to never-smokers. Women diagnosed with cancer of the upper respiratory organs were ineligible for selection as controls. Personal interviews of cases and controls were conducted in the hospital wards, using a closed-form structured questionnaire. An elevated risk of lung cancer was observed in women whose husbands smoked. The odds ratio (OR) adjusted by age and education for husband's smoking was 1.53 (95% CI, 1.06-2.21). Smoking by other members of the family, by colleague's, or by fathers in the women's childhood do not affect the risk of lung cancer. The risk is higher for women whose husbands smoke "papirosy" (OR 2.12; 95% CI, 1.32-3.40), a special Russian type of cigarettes with a long mouthpiece, and usually very high levels of tar (> 30 mg/cig) and nicotine (> 1.8 mg/cig). Our study suggests that the association between exposure to ETS of the spouse and risk of lung cancer in non-smoking women is somewhat stronger for squamous-cell carcinoma (OR, 1.94; 95% CI, 0.99-3.81) than for adenocarcinoma (OR, 1.52; 95% CI, 0.96-2.39).
 ...
PMID:Exposure to environmental tobacco smoke and risk of lung cancer in non-smoking women from Moscow, Russia. 945 89

To examine the relationship between exposure to passive smoke (herein referred to as environmental tobacco smoke, ETS), cooking fumes, other risk factors and primary adenocarcinoma of the lung, 70 adenocarcinoma lung cancer cases of non-smoking women in Nanjing were studied in a 1:1 case-control study. Results show no statistical association between exposure to ETS and pulmonary adenocarcinoma. The respective odds ratios for chronic lung disease, cooking fume pollution and family tumor history were 3.90, 2.45 and 4.36.
 ...
PMID:Relation of exposure to environmental tobacco smoke and pulmonary adenocarcinoma in non-smoking women: a case control study in Nanjing. 968 39

This paper presents a model to estimate the number of lung cancer deaths due to ETS exposure among the 1992 U.S. never-smoking population, based on downward linear extrapolation from the estimated risks of active smokers. The model uses several recently available data sources including an extensive review of the published literature on indoor concentration of ETS constituents measured under real-world conditions and data from the National Mortality Followback Survey and the National Health Interview Survey which furnish nationally representative estimates of the distribution of the U.S. population and the persons who died from lung cancer by sex, age, and smoking status. The linear extrapolation model estimates that five male and six female excess lung cancer deaths due to ETS exposure would be expected in the 1992 U.S. population of over 52 million never smokers age 35 and over. Explanations for differences between the results of our downward extrapolation model and those of others are presented.
 ...
PMID:Linear extrapolation models of lung cancer risk associated with exposure to environmental tobacco smoke. 992 60

Factors that affect the risk of lung adenocarcinoma among females were investigated in Shenyang, China, using a population-based case-control study design. A total of 72 new cases, ages 35-69, diagnosed with incident, primary pulmonary adenocarnoma, were collected between April 1991 and December 1995, and were 1:1 age-matched with healthy females randomly selected from the general population. A questionnaire covering demographics, diet/nutritional preferences and cooking habits, living conditions, family history of cancer, sources of indoor/outdoor/occupational pollution, exposure to ETS from spousal smoking, workplace exposure, and exposure during childhood, history of menstruation and pregnancy, was given to each subject in a structured in-person interview given by trained field workers. Univariate analysis was performed on the data collected. The results showed that cooking fumes, family history of lung cancer, economic status, and number of live births and intake of vitamin E were risk factors significantly associated with adenocarcinoma of the lung. In particular, exposure to different levels of cooking fumes, an indoor air pollutant, increased the odds ratio of lung adenocarcinoma by 1.33, 7.33 and 1.67, respectively (trend p=0.006). Another important risk factor was family history of lung cancer, which gave an OR of 7.65 (95% CI, 0.90-169.84). Intake of beta-carotene from vegetables and fruit offered protection against lung adenocarcinoma, giving an OR of 0.28 (95% CI, 0.12-0.69). These results were confirmed by multivariable logistic regression analysis.
 ...
PMID:Indoor air pollution and pulmonary adenocarcinoma among females: a case-control study in Shenyang, China. 1103 25

ETS contains numerous toxins. Robust epidemiologic evidence implicates ETS as a cause of lung cancer and as a primary cause and source of exacerbation of excess respiratory disease. There is also increasing evidence that ETS may be associated with other outcomes, including heart disease. There is currently little doubt that ETS is an important and avoidable health hazard. Unfortunately, ETS is frequently encountered in the workplace--where it is no safer than in other environments and where it presents hazards to exposed workers and to others. A unique aspect of workplace ETS is that exposure is rarely an outcome of essential manufacturing, extraction, or service delivery processes. Moreover, ETS exposure, with its growing list of known hazards, is preventable by engineering or policy means. Implementation of policies to prevent workplace ETS can be highly effective while entailing low costs and yielding primary and secondary benefits to employers and employees. ACOEM strongly supports an increase in the scope and effectiveness of policies and efforts that protect against exposure to ETS in the workplace and elsewhere. To that end, ACOEM supports voluntary, regulatory, and legislative initiatives to eliminate ETS from the workplace, including public spaces such as bars, casinos, restaurants, schools, day-care centers, and public transportation. ACOEM also encourages employers to provide employee training concerning the health hazards of ETS and voluntary personal smoking-cessation programs.
 ...
PMID:Epidemiologic basis for an occupational and environmental policy on environmental tobacco smoke. 1112 75


1 2 3 4 Next >>