Heart Disease From Passive Smoking in the Workplace

Wells, A. Judson

doi:10.1016/s0735-1097(97)00432-4

Cited by 75 publications

(42 citation statements)

References 25 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…Tobacco smoking has a pressing effect on the vessels, resulting in the development of arterial hypertension. Results of meta-analyses performed by several independent research centres have revealed a connection between passive smoking and CVD [20][21][22][23][24][25]. Low level of physical activity was the next problem in the population examined in our study; 46% of the participants (42% men and 54% women) did not practise any kind of physical activity during leisure time.…”

Section: Psychological Factorsmentioning

confidence: 68%

Work-related risk factors of myocardial infarction

Bortkiewicz

Gadzicka²,

Siedlecka³

et al. 2010

International Journal of Occupational Medicine and Environmental Health

View full text Add to dashboard Cite

Objectives: The aim of the study was to find out which occupational factors account for the risk of the myocardial infarction. Material and Methods: A questionnaire survey was performed during the period of one calendar year in all patients (1053 subjects, 692 men and 361 women) hospitalized at the Medical University of Łódź because of the first myocardial infarction. The questionnaire was prepared especially for the purpose of this study and consisted of two parts. The first part comprised: demographic data, health status at admittance, traditional risk factors for the ischaemic heart disease and was filled-in by physicians. Part II was done by occupational hygiene specialists and referred to education, job title and characteristics, employment data, self assessment of work-related and general stress, fatigue, socio-economic status, physical activity, alcohol intake, tobacco smoking, dietary habits. Results: Mean age in the study group was 59.9±10.4 years (26-85 years), 58.7±10.0 (26-84 years) for men and 62.3±10.7 (32-85 years) for women, employment duration was 32.9±8.8 (4-65 years), for men 34.0±8.6 (5-65 years), for women 30.7±8.8 (4-60 years. Most of myocardial infarction cases both in the group of men and women were noted in the age interval 56-60 years, 22.3% vs. 17.4%, respectively. The majority of examined men were farmers, low and middle management and self-employed workers. Among women prevailed clerks, seamstresses and farmers. The most frequent occupational risk factors were: work-related stress, experienced by 54.2% of the examined subjects, occupational noise (45,5%), dust (41,7%) and various chemical factors (33%). A majority of the study group (76.5% women and 54.4% men) linked the cardiac infarction with stress, while 39.1% men vs. 16.5% women correlated it with physical effort. Conclusion: Our studies indicate that, among a wide spectrum of occupational factors, stress, noise and fine particulate dust are major contributors to the increased risk of myocardial infarction.

show abstract

Section: Psychological Factorsmentioning

confidence: 68%

Work-related risk factors of myocardial infarction

Bortkiewicz

Gadzicka²,

Siedlecka³

et al. 2010

International Journal of Occupational Medicine and Environmental Health

View full text Add to dashboard Cite

show abstract

“…Several reports, including 2 recent separate meta-analyses of 17 and 18 individual studies, assessed the association of SHS with heart disease. 20,[51][52][53] Both estimated that nonsmoking spouses of smoking partners experience an approximately 25% (95% confidence interval [CI] 17% to 32%) increased risk of heart disease. 52,53 A review of 6 studies examining the association between SHS in the workplace and cardiovascular disease noted that although none of the studies individually reached the level of a significant association (PϽ0.05), there was a positive association in 5 of the 6 studies and a significant exposureresponse relation between the intensity of SHS (measured by the number of cigarettes smoked by coworkers) and coronary risk in 2 of 3 studies that examined the trend.…”

Section: Secondhand Smokementioning

confidence: 99%

Air Pollution and Cardiovascular Disease

Brook¹,

Franklin²,

Cascio³

et al. 2004

Circulation

1,977

819

View full text Add to dashboard Cite

Abstract-Air pollution is a heterogeneous, complex mixture of gases, liquids, and particulate matter. Epidemiological studies have demonstrated a consistent increased risk for cardiovascular events in relation to both short-and long-term exposure to present-day concentrations of ambient particulate matter. Several plausible mechanistic pathways have been described, including enhanced coagulation/thrombosis, a propensity for arrhythmias, acute arterial vasoconstriction, systemic inflammatory responses, and the chronic promotion of atherosclerosis. The purpose of this statement is to provide healthcare professionals and regulatory agencies with a comprehensive review of the literature on air pollution and cardiovascular disease. In addition, the implications of these findings in relation to public health and regulatory policies are addressed. Practical recommendations for healthcare providers and their patients are outlined. In the final section, suggestions for future research are made to address a number of remaining scientific questions. Key Words: AHA Scientific Statements Ⅲ air pollution Ⅲ cardiovascular diseases Ⅲ respiration R ecently, the American Heart Association (AHA) published "Guidelines for Primary Prevention of Cardiovascular Disease and Stroke" as an aid to healthcare professionals and their patients without established coronary artery disease or other atherosclerotic diseases. 1 The statement was intended to complement the AHA/American College of Cardiology (ACC) "Guidelines for Preventing Heart Attack and Death in Patients with Atherosclerotic Cardiovascular Disease." 2 Both sets of recommendations emphasized multifactorial interventions, especially more intensive measures/ goals to modify individual cardiovascular risk factors with diet, drugs, exercise, weight management, complete smoking cessation, and avoidance of secondhand smoke (SHS), or combinations thereof.Over the last decade, however, a growing body of epidemiological and clinical evidence has led to a heightened concern about the potential deleterious effects of ambient air pollution on health and its relation to heart disease and stroke. Of special interest are several environmental air pollutants that include carbon monoxide, oxides of nitrogen, sulfur dioxide, ozone, lead, and particulate matter ("thoracic particles" [PM 10 ] Ͻ10 m in aerodynamic diameter, "fine particles" [PM 2.5 ] Ͻ2.5 m, and "coarse particles" [PM 10 to 2.5 ]). These pollutants are associated with increased hospitalization 3 and mortality due to cardiovascular disease, 4 -6 especially in persons with congestive heart failure, frequent arrhythmias, or both. 7 The well-established causal associations between active and passive smoking with heart disease and stroke support the plausibility of an adverse effect of PM on the cardiovascular system.The most recent analysis of the National Mortality and Morbidity Air Pollution Study (NMMAPS), based on data from 90 of the largest cities in the United States, estimated that daily total and cardiopulmonary mortality incr...

show abstract

“…Based on pooled analyses of epidemiologic studies, nonsmokers exposed to ETS in the workplace have an estimated cardiovascular risk 1.35 times that of those not exposed, whereas those exposed at home have a cardiovascular risk 1.23 times that of the unexposed (4). Should these estimates be accurate, ETS exposure would rank as the third leading cause of avoidable death in the United States (1).…”

Section: Introductionmentioning

confidence: 99%

Why Is Environmental Tobacco Smoke More Strongly Associated with Coronary Heart Disease Than Expected? A Review of Potential Biases and Experimental Data

Howard¹,

Thun²

1999

Environmental Health Perspectives

View full text Add to dashboard Cite

Despite exposure levels estimated to be equivalent to smoking only 0.1-1.0 cigarettes per day, exposure to environmental tobacco smoke (ETS) is estimated to increase the risk of death from coronary heart disease (CHD) between 25 and 35% above the risk of nonexposed persons. This surprisingly large risk associated with a seemingly small exposure has raised doubts about the validity of attributing the increased CHD risk to ETS exposure. This paper reviews various biases that have been hypothesized to account for the increased CHD risk associated with ETS in the epidemiologic studies and characterizes the adverse effects of ETS on thrombosis, vascular endothelium, and exercise tolerance observed in experimental studies of humans and laboratory animals. None of the identified factors that has been proposed to introduce a spurious association between ETS and heart disease seem to invalidate the epidemiologic findings, either separately or in combination. In addition, experimental studies of ETS and heart disease demonstrate that acute exposure of humans and other species to ETS affects platelet function, vascular endothelium, and myocardial exercise tolerance at exposure concentrations widely prevalent in the workplace. Because exposure to ETS affects multiple physiologic pathways, it appears biologically plausible that ETS could cause the substantial increase in CHD risk that has been observed in epidemiologic studies. Key words: atherosclerosis, cardiovascular disease, risk factor, smoking. -Environ Health Perspect 1 07(suppl 6): 853-858 (1999). http.//ehpnet 1. niehs. nih.gov/docs/1999/suppl-6/853-858howard/abstract. html

show abstract

Heart Disease From Passive Smoking in the Workplace

Abstract: The RRs for heart disease from passive smoking at work are roughly equal to those from home-based exposure.

Cited by 75 publications

References 25 publications

Work-related risk factors of myocardial infarction

Work-related risk factors of myocardial infarction

Air Pollution and Cardiovascular Disease

Why Is Environmental Tobacco Smoke More Strongly Associated with Coronary Heart Disease Than Expected? A Review of Potential Biases and Experimental Data

Contact Info

Product

Resources

About