{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,4]],"date-time":"2026-10-04T23:40:14Z","timestamp":1791157214857,"version":"4.1.0"},"reference-count":94,"publisher":"BMJ","issue":"7114","license":[{"start":{"date-parts":[[1997,10,18]],"date-time":"1997-10-18T00:00:00Z","timestamp":877132800000},"content-version":"tdm","delay-in-days":0,"URL":"http:\/\/www.bmj.com\/company\/legal-information\/terms-conditions\/legal-information\/tdm-licencepolicy"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["BMJ"],"accepted":{"date-parts":[[1997,9,23]]},"published-print":{"date-parts":[[1997,10,18]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:p>\n                    <jats:bold>Objectives:<\/jats:bold>\n                    To estimate the risk of ischaemic heart disease caused by exposure to environmental tobacco smoke and to explain why the associated excess risk is almost half that of smoking 20 cigarettes per day when the exposure is only about 1% that of smoking.\n                  <\/jats:p>\n                  <jats:p>\n                    <jats:bold>Design:<\/jats:bold>\n                    Meta-analysis of all 19 acceptable published studies of risk of ischaemic heart disease in lifelong non-smokers who live with a smoker and in those who live with a non-smoker, five large prospective studies of smoking and ischaemic heart disease, and studies of platelet aggregation and studies of diet according to exposure to tobacco smoke.\n                  <\/jats:p>\n                  <jats:p>\n                    <jats:bold>Results:<\/jats:bold>\n                    The relative risk of ischaemic heart disease associated with exposure to environmental tobacco smoke was 1.30 (95% confidence interval 1.22 to 1.38) at age 65. At the same age the estimated relative risk associated with smoking one cigarette per day was similar (1.39 (1.18 to 1.64)), while for 20 per day it was 1.78 (1.31 to 2.44). Two separate analyses indicated that non-smokers who live with smokers eat a diet that places them at a 6% higher risk of ischaemic heart disease, so the direct effect of environmental tobacco smoke is to increase risk by 23% (14% to 33%), since 1.30\/1.06=1.23. Platelet aggregation provides a plausible and quantitatively consistent mechanism for the low dose effect. The increase in platelet aggregation produced experimentally by exposure to environmental tobacco smoke would be expected to have acute effects increasing the risk of ischaemic heart disease by 34%.\n                  <\/jats:p>\n                  <jats:p>\n                    <jats:bold>Conclusion:<\/jats:bold>\n                    Breathing other people's smoke is an important and avoidable cause of ischaemic heart disease, increasing a person's risk by a quarter.\n                  <\/jats:p>\n                  <jats:p>\n                    <jats:boxed-text position=\"float\">\n                      <jats:sec>\n                        <jats:title>Key messages<\/jats:title>\n                        <jats:list list-type=\"bullet\">\n                          <jats:list-item>\n                            <jats:p>Analysis of 19 epidemiological studies shows that people who have never smoked have an estimated 30% greater risk of ischaemic heart disease if they live with a smoker (P&lt;0.001)<\/jats:p>\n                          <\/jats:list-item>\n                          <jats:list-item>\n                            <jats:p>This is surprisingly large\u2014almost half the risk of smoking 20 cigarettes per day even though the exposure is only 1% of that of a smoker<\/jats:p>\n                          <\/jats:list-item>\n                          <jats:list-item>\n                            <jats:p>The excess risk from smoking one cigarette per day is 39%\u2014similar to the risk in a non-smoker living with a smoker<\/jats:p>\n                          <\/jats:list-item>\n                          <jats:list-item>\n                            <jats:p>The effect is mainly explained by a non-linear dose-response relation between expsoure to tobacco smoke and risk of heart disease<\/jats:p>\n                          <\/jats:list-item>\n                          <jats:list-item>\n                            <jats:p>Detailed analysis shows no significant bias; dietary confounding can account for an excess risk of only 6%, so revising the excess risk from 30% to 23%<\/jats:p>\n                          <\/jats:list-item>\n                        <\/jats:list>\n                      <\/jats:sec>\n                    <\/jats:boxed-text>\n                  <\/jats:p>","DOI":"10.1136\/bmj.315.7114.973","type":"journal-article","created":{"date-parts":[[2011,10,27]],"date-time":"2011-10-27T19:49:09Z","timestamp":1319744949000},"page":"973-980","source":"Crossref","is-referenced-by-count":383,"title":["Environmental tobacco smoke exposure and ischaemic heart disease: an evaluation of the evidence"],"prefix":"10.1136","volume":"315","author":[{"given":"M R","family":"Law","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"J K","family":"Morris","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"N J","family":"Wald","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"239","published-online":{"date-parts":[[1997,10,18]]},"reference":[{"key":"2025122508333335000_315.7114.973.1","doi-asserted-by":"crossref","first-page":"1","DOI":"10.1161\/01.CIR.83.1.1","article-title":"Passive smoking and heart disease: epidemiology, physiology and biochemistry.","volume":"83","author":"Glantz","year":"1991","journal-title":"Circulation"},{"key":"2025122508333335000_315.7114.973.2","doi-asserted-by":"publisher","DOI":"10.1016\/0735-1097(94)90315-8"},{"key":"2025122508333335000_315.7114.973.3","doi-asserted-by":"crossref","first-page":"1047","DOI":"10.1001\/jama.1995.03520370089043","article-title":"Passive smoking and heart disease: mechanisms and risk.","volume":"273","author":"Glantz","year":"1995","journal-title":"JAMA"},{"key":"2025122508333335000_315.7114.973.4","doi-asserted-by":"publisher","DOI":"10.1001\/jama.1992.03480010102033"},{"key":"2025122508333335000_315.7114.973.5","doi-asserted-by":"crossref","first-page":"1942","DOI":"10.1001\/archinte.1995.00430180034005","article-title":"Passive smoking and cardiovascular risk.","volume":"155","author":"Kritz","year":"1995","journal-title":"Arch Intern Med"},{"key":"2025122508333335000_315.7114.973.6","doi-asserted-by":"crossref","first-page":"167","DOI":"10.1080\/00039896.1969.10666825","article-title":"Coronary heart disease, stroke, and aortic aneurysm.","volume":"19","author":"Hammond","year":"1969","journal-title":"Arch Environ Health"},{"key":"2025122508333335000_315.7114.973.7","unstructured":"Hammond EC . 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