{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,1]],"date-time":"2026-10-01T07:07:19Z","timestamp":1790838439704,"version":"4.1.0"},"reference-count":30,"publisher":"Wiley","issue":"4","license":[{"start":{"date-parts":[[2014,1,1]],"date-time":"2014-01-01T00:00:00Z","timestamp":1388534400000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["Acta Paediatrica"],"published-print":{"date-parts":[[2014,4]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:sec><jats:title>Aim<\/jats:title><jats:p>To compare blood pressure reactions (<jats:styled-content style=\"fixed-case\">BPR<\/jats:styled-content>) of infants to mild stress for evidence of adverse cardiovascular effects of passive exposure to tobacco smoke during pregnancy and early infancy.<\/jats:p><\/jats:sec><jats:sec><jats:title>Methods<\/jats:title><jats:p>An observational field study conducted in Crete. We compared 4\u2010 to 6\u2010month olds of lifelong nonsmokers minimally (controls, n\u00a0=\u00a09) or frequently exposed to tobacco smoke (passive smokers; n\u00a0=\u00a010) with those born to habitual smokers (n\u00a0=\u00a06). Smoke exposure was verified biochemically (urine cotinine each trimester and at study). We recorded beat\u2010to\u2010beat blood pressure (<jats:styled-content style=\"fixed-case\">BP<\/jats:styled-content>) during brief repositioning manoeuvres performed during a daytime nap and analysed <jats:styled-content style=\"fixed-case\">BPR<\/jats:styled-content> (% change in <jats:styled-content style=\"fixed-case\">BP<\/jats:styled-content> during head\u2010up tilt) for associations with maternal and infant cotinine.<\/jats:p><\/jats:sec><jats:sec><jats:title>Results<\/jats:title><jats:p>We observed a 20\u2010fold difference between <jats:styled-content style=\"fixed-case\">BPR<\/jats:styled-content> of infants of controls versus passive smokers \u2013 exceptional given number of infants (\u03b1 error\/confidence level &lt;10% i.e. power &gt;90%). The <jats:styled-content style=\"fixed-case\">BPR<\/jats:styled-content> declined linearly as the infant's (but not mother's) cotinine level rose (p\u00a0=\u00a00.04), indicating abnormal <jats:styled-content style=\"fixed-case\">BPR<\/jats:styled-content> was caused mainly by postnatal smoke exposure. Infants of active smokers differed from those of passive smokers.<\/jats:p><\/jats:sec><jats:sec><jats:title>Conclusion<\/jats:title><jats:p>Cardiovascular effects of passive smoking by a newborn infant manifest early on and are exceptionally strong. They can be largely avoided by keeping the home smoke rigorously free.<\/jats:p><\/jats:sec>","DOI":"10.1111\/apa.12538","type":"journal-article","created":{"date-parts":[[2013,12,12]],"date-time":"2013-12-12T19:12:52Z","timestamp":1386875572000},"page":"386-392","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":5,"title":["Adverse circulatory effects of passive smoking during infancy: surprisingly strong, manifest early, easily avoided"],"prefix":"10.1111","volume":"103","author":[{"given":"G","family":"Cohen","sequence":"first","affiliation":[{"name":"Department of Women's and Children's Health Karolinska Institute Stockholm Sweden"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"C","family":"Vardavas","sequence":"additional","affiliation":[{"name":"Department of Social Medicine University of Crete Heraklion Greece"},{"name":"Center for Global Tobacco Control Harvard School of Public Health Boston MA 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