Skip to main page content
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
. 2011:2011:854584.
doi: 10.1155/2011/854584. Epub 2011 May 29.

Paternal smoking and risk of childhood acute lymphoblastic leukemia: systematic review and meta-analysis

Ruiling Liu  1 , Luoping Zhang, Cliona M McHale, S Katharine Hammond
Affiliations

Paternal smoking and risk of childhood acute lymphoblastic leukemia: systematic review and meta-analysis

Ruiling Liu et al. J Oncol. 2011.

Abstract

Objective. To investigate the association between paternal smoking and childhood acute lymphoblastic leukemia (ALL). Method. We identified 18 published epidemiologic studies that reported data on both paternal smoking and childhood ALL risk. We performed a meta-analysis and analyzed dose-response relationships on ALL risk for smoking during preconception, during pregnancy, after birth, and ever smoking. Results. The summary odds ratio (OR) of childhood ALL associated with paternal smoking was 1.11 (95% Confidence Interval (CI): 1.05-1.18, I(2) = 18%) during any time period, 1.25 (95% CI: 1.08-1.46, I(2) = 53%) preconception; 1.24 (95% CI: 1.07-1.43, I(2) = 54%) during pregnancy, and 1.24 (95% CI: 0.96-1.60, I(2) = 64%) after birth, with a dose-response relationship between childhood ALL and paternal smoking preconception or after birth. Conclusion. The evidence supports a positive association between childhood ALL and paternal ever smoking and at each exposure time period examined. Future epidemiologic studies should assess paternal smoking during well-defined exposure windows and should include biomarkers to assess smoking exposure and toxicological mechanisms.

PubMed Disclaimer

Figures

Figure 1
Figure 1
Meta-analysis of the association between childhood ALL and paternal smoking in different time windows. Random-effect OR estimates and weights were used in the graphs. X-axis represent the OR (odds ratio). The sizes of the boxes indicate the weight of the corresponding study used for estimates of summary effects.
Figure 2
Figure 2
Begg's funnel plots of the log odds ratio (ln(OR)) versus the standard error of the log odds ratio (s.e of ln(OR)) of the studies used in the meta-analysis. Random-effect model OR estimates were used in the graphs. The sizes of the circles indicate the inverse-variance weight of the corresponding study.
Figure 3
Figure 3
Clear positive dose-response associations between paternal smoking and childhood ALL found from the literature. Note: Among all the 18 studies included in this meta-analysis, two did not present dose-response analysis [32, 43], 10 did not find clear dose-response trend, and the remaining six studies reported clear dose-response trends [23, 33, 35, 37, 41, 42], which were presented in this figure. CPD: cigarettes per day; PY: pack years; the figure for Chang et al. 2006 [23] was estimated from their report that, for paternal preconception smoking, an OR of 1.03 (95% CI: 1.00–1.06) was associated with a one-CPD increment, and an OR of 1.34 (95% CI: 1.02–1.74) with 10-CPD increment, and the figure for Sorahan et al. 1995 [35] was estimated from their report of an OR of 1.16 (95% CI: 1.06–1.27) for change of one level of prenatal use of tobacco products.
Figure 4
Figure 4
Evaluation of dose-response relationships between paternal smoking at different time windows and childhood ALL risk. Estimates by random-effect models were used when between-study heterogeneity was statistically significant; CPD: cigarettes per day; before pregnancy dose-response analysis was based on eight studies [–30, 33, 34, 37, 43], during pregnancy analysis was based on four studies [–29, 33] and after birth analysis was based on four studies [26, 30, 31, 33]; The risk estimates for exposure to paternal smoking with 10–19 CPD and with ≥20 CPD were combined to get estimates on exposure to paternal smoking with <20 CPD from Rudant et al. 2008 [33] and from Menegaux et al. 2005 [31]; *includes exposure to paternal smoking of 1–15 CPD (OR = 0.9, 95% CI: 0.6–1.5) up to child's birth, **includes exposure to paternal smoking of >16 CPD (OR = 0.9, 95% CI: 0.5–1.6) up to child's birth, as reported by Magnani et al. 1990 [29]; The dose-response analysis in Sorahan's paper in 2001 [37] was based on exposure categories of: lifelong nonsmokers, <10, 10–19, 20–29, 30–39, and ≥40 CPD during preconception, the later three categories were combined using the raw data for the purpose of this meta-analysis.
See this image and copyright information in PMC

Similar articles

See all similar articles

Cited by

See all "Cited by" articles

References

    1. American Cancer Society. What are the key statistics for childhood leukemia. 2010, http://www.cancer.org/Cancer/LeukemiainChildren/DetailedGuide/childhood-....
    1. Smith MA, et al. Leukemia. SEER Pediatric Monograph. 2010, http://seer.cancer.gov/publications/childhood/leukemia.pdf.
    1. Surveillance Epidemiology and End Results (SEER) SEER Cancer Statistics Review 1975–2007. 2010, http://seer.cancer.gov/csr/1975_2007/results_single/sect_28_table.09.pdf.
    1. World Health Organization. Disease and injury regional estimates for 2004. 2010, http://www.who.int/healthinfo/global_burden_disease/estimates_regional/e....
    1. Greaves M. Science, medicine, and the future: childhood leukaemia. British Medical Journal. 2002;324(7332):283–287. - PMC - PubMed

LinkOut - more resources