一項(xiàng)由澳大利亞研究人員完成，發(fā)表在The American Journal of Epidemiology上的研究"Parental Prenatal Smoking and Risk of Childhood Acute Lymphoblastic Leukemia"顯示：如果爸爸經(jīng)常在孩子周圍抽煙，那么孩子患兒童癌癥（白血病的一種）的風(fēng)險(xiǎn)至少會提高15%,。
同時(shí)這項(xiàng)研究顯示,，急性淋巴細(xì)胞白血?。ˋLL）是由多重因素引起的，
“研究結(jié)果表明,，有一個(gè)‘老煙槍’爸爸,，是孩子患ALL的風(fēng)險(xiǎn)因子之一。”由來自澳大利亞兒童健康研究院的Elizabeth Milne領(lǐng)銜的研究者們寫道,。
盡管ALL是兒童中最常見的癌癥,，但它的發(fā)病率依然很低，100,000個(gè)孩子當(dāng)中大概只有3~5個(gè)會患此病,。
研究者們對將近300個(gè)患有ALL孩子的家庭進(jìn)行了調(diào)查,，并對其父母雙方的抽煙習(xí)慣進(jìn)行了統(tǒng)計(jì)。他們還將這些家庭與另外800多個(gè)未患ALL的孩子的家庭進(jìn)行比較,。
研究者們發(fā)現(xiàn),，媽媽的抽煙行為并不會增加孩子患ALL的風(fēng)險(xiǎn)，但是如果在孩子印象里爸爸一直在其周圍抽煙的話,，他們患ALL的風(fēng)險(xiǎn)至少會增加15%,。
更可怕的是，那些爸爸一天至少要抽20根煙的孩子被診斷出ALL的風(fēng)險(xiǎn)甚至增加到44%,。
“長期生活在吸煙環(huán)境中與孩子得癌癥之間的關(guān)聯(lián)直到近期才為人們所知,。” 研究者之一、來自加州大學(xué)的Patricia Buffler說,。
她補(bǔ)充道，既然煙草中飽含毒素,，包括致癌原,，所以它會損傷產(chǎn)生精子的細(xì)胞也不無可能。
Milne也表示贊同,，她說：“精子中含有DNA（易受損傷）,，在與卵子結(jié)合之后，就可能將疾病帶給下一代,。”
但是,，她又補(bǔ)充道，這項(xiàng)研究并沒有證明精子DNA損傷會導(dǎo)致兒童患ALL,，而且這種疾病是由多個(gè)因素造成的,。
其他極有可能導(dǎo)致兒童患上ALL的環(huán)境因素還包括致電離輻射（如X射線）以及媽媽在懷孕期間長期暴露于涂料和殺蟲劑環(huán)境中。（生物谷bioon.com）
doi:10.1093/aje/kwr275
PMC:
PMID:
Parental Prenatal Smoking and Risk of Childhood Acute Lymphoblastic Leukemia
Elizabeth Milne, Kathryn R. Greenop, Rodney J. Scott, Helen D. Bailey, John Attia, Luciano Dalla-Pozza, Nicholas H. de Klerk and Bruce K. Armstrong
The association between parental smoking and risk of childhood acute lymphoblastic leukemia (ALL) was investigated in an Australian population-based case-control study that included 388 cases and 868 controls aged <15 years, recruited from 2003 to 2006. Both of the child’s parents provided information about their smoking habits for each year from age 15 years to the child’s birth. Data were analyzed by logistic regression. Maternal smoking was not associated with risk of childhood ALL, but the odds ratio for paternal smoking of ≥15 cigarettes per day around the time of the child’s conception was 1.35 (95% confidence interval: 0.98, 1.86). The associations between parental smoking risk of childhood ALL did not differ substantially by immunophenotypic or cytogenetic subtype. Meta-analyses of paternal smoking, including results from the Australian Study of Causes of Acute Lymphoblastic Leukemia in Children and those of previous studies, produced summary odds ratios of 1.15 (95% confidence interval: 1.06, 1.24) for any paternal smoking around the time of the child’s conception and 1.44 (95% confidence interval: 1.24, 1.68) for smoking ≥20 cigarettes per day at that time. Study results suggest that heavier paternal smoking around the time of conception is a risk factor for childhood ALL. Men should be strongly encouraged to cease smoking, particularly when planning to start a family.
