Department of Hygiene and Public Health, Nippon Medical School
Corresponding Author: Tomoyuki Kawada, Department of Hygiene and Public Health, Nippon Medical School, 1-1-5 Sendagi, Bunkyo-Ku, Tokyo 113-8602, Japan, email@example.com
J Prev Alz Dis 2021;
Published online September 13, 2021, http://dx.doi.org/10.14283/jpad.2021.51
Key words: Secondhand smoke, dementia, Alzheimer’s disease; stroke; risk assessment.
I read the paper by Zhou et al. with great interest (1). The authors conducted a long-term follow-up study to investigate the associations between exposure to secondhand smoke and the subsequent risk of dementia, Alzheimer’s disease (AD), and stroke (1). The adjusted hazard ratios (HRs; 95% confidence intervals [CIs]) of the highest exposure to secondhand smoke compared to individuals with no exposure for dementia, AD, and stroke were 2.86 (2.00–4.09), 3.13 (1.80–5.42), and 1.89 (1.37–2.61), respectively. In addition, a dose–response relationship was also observed in this study. I would like to present some information relevant to their study.
First, Rovio et al. also conducted a long-term follow-up study to evaluate the association between exposure to parental smoking during childhood/adolescence and midlife cognitive function (2). They classified the participants into three groups: G1) nonsmoking parents with the participants’ serum cotinine level <1.0 ng/mL; G2) 1–2 smoking parents with the participants’ serum cotinine level <1.0 ng/mL; and G3) 1–2 smoking parents with the participants’ serum cotinine level ≥1.0 ng/mL. Compared to participants in group G1, the relative risk (RR; 95% CI) of those in group G3 for midlife episodic memory and associative learning was 1.38 (1.08–1.75), and they were advised to avoid exposure to secondhand smoke during childhood/adolescence to maintain cognitive function in adulthood. This report was based on valid data with exposure to parental smoking evaluated by assessment of serum cotinine levels, and the RR (95% CI) of participants in group G3 for short-term and spatial working memory was 1.25 (0.98–1.58), presenting a tendency of the association. Although this report did not select dementia and AD as clinical outcomes, midlife cognitive impairment is closely related to the subsequent risk of dementia and AD.
Second, Pistilli et al. evaluated the association between exposure to secondhand smoke during childhood and the subsequent risk of stroke or coronary heart disease (CHD) among never-smokers (3). The adjusted HRs (95% CI) of ≥2 childhood household smokers for stroke and CHD were 1.66 (1.29–2.13) and 1.15 (0.82–1.59), respectively. Although the type of stroke could not be specified, a long-term effect of secondhand smoke on the risk of stroke was observed, which was consistent with the data presented by Zhou et al. Further studies are required to verify the association between stroke and the risk of dementia and AD.
The pathology of AD begins a few decades before onset of the clinical symptoms, and there are some modifiable risk and protective factors (4). In any case, comprehensive studies are required to verify the associations of lifestyle factors with dementia, AD, and stroke subtypes.
Conflict of interest: None declared.
1. Zhou S, Wang K. Childhood secondhand smoke exposure and risk of dementia, Alzheimer’s disease and stroke in adulthood: A prospective cohort study. J Prev Alzheimers Dis 2021;8(3):345-350, https://doi.org/10.14283/jpad.2021.10.
2. Rovio SP, Pihlman J, Pahkala K, et al. Childhood exposure to parental smoking and midlife cognitive function. Am J Epidemiol 2020;189(11):1280-129, https://doi.org/10.1093/aje/kwaa052.
3. Pistilli M, Howard VJ, Safford MM, et al. Association of secondhand tobacco smoke exposure during childhood on adult cardiovascular disease risk among never-smokers. Ann Epidemiol 2019;32:28-34.e1, https://doi.org/10.1016/j.annepidem.2019.01.012.
4. Zhang XX, Tian Y, Wang ZT, et al. The epidemiology of Alzheimer’s disease modifiable risk factors and prevention. J Prev Alzheimers Dis 2021;8(3):313-32, https://doi.org/10.14283/jpad.2021.15.