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BackgroundThe association between exposure to secondhand smoke (SHS) during pregnancy and a child’s neurodevelopment has not been established yet. We explored the association between prenatal exposure to SHS and neurodevelopment at 24 months of age considering genetic polymorphism and breastfeeding in 720 mothers and their offspring enrolled in the Korean multicenter birth cohort study (Mothers and Children Environmental Health, MOCEH).MethodsWe quantified urine cotinine concentrations in mothers once from 12th to 20th gestational weeks and excluded those whose urine cotinine levels exceeded 42.7 ng/ml to represent SHS exposure in early pregnancy. Mental developmental index (MDI) and psychomotor developmental index (PDI) values were measured using the Korean version of the Bayley Scales of Infant Development II (K-BSID-II) at 24 months of age. A general linear model was used to assess the relationship between maternal urinary cotinine level and neurodevelopment.ResultsMDI scores were inversely associated with cotinine [β = − 2.73; 95% confidence interval (CI): − 5.32 to − 0.15] in children whose mothers had early pregnancy urinary cotinine levels >1.90 ng/ml. No association was evident in children whose mothers had cotinine levels ≤1.90 ng/ml. This negative association was more pronounced in children whose mothers had both Glutathione S-transferases mu 1 (GSTM1) and theta 1 (GSTT1) null type [β = − 5.78; 95% CI: -10.69 to − 0.87], but not in children whose mothers had any present type of GSTM1/GSTT1 [β = − 1.64; 95% CI: -4.79 to 1.52]. The association was no longer significant when children received breast milk exclusively for up to 6 months [β = − 0.24; 95% CI: -4.69 to 4.20] compared to others [β = − 3.75; 95% CI: -7.51 to 0.00]. No significant association was found for PDI.ConclusionsMaternal exposure to SHS during pregnancy may result in delayed MDI in early childhood. This effect might be modified by genetic polymorphism and breastfeeding behavior.Electronic supplementary materialThe online version of this article (10.1186/s12940-019-0463-9) contains supplementary material, which is available to authorized users.

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Key Points Question Is long-term use of low-dose aspirin associated with reduced risk of lung cancer, and if so, which populations may derive the greatest benefit? Findings This cohort study using data from 12 969 400 participants in the Korean National Health Information Database found that the use of low-dose aspirin for more than 5 years was associated with a modest risk reduction of incident lung cancer, with the strongest association observed among elderly participants and among people without diabetes. Meaning Intake of low-dose aspirin for more than 5 years may reduce the risk of incident lung cancer, particularly among the elderly and among people without diabetes.

Family history of cancer is a well-known risk factor but the role of family history in survival is less clear. The aim of this study was to investigate the association between family history and cancer survival for the common cancers in Sweden. Using the Swedish population-based registers, patients diagnosed with the most common cancers were followed for cancer-specific death during 1991-2010. We used multivariate proportional hazards (Cox) regression models to contrast the survival of patients with a family history of cancer (individuals whose parent or sibling had a concordant cancer) to the survival of patients without a family history. Family history of cancer had a modest protective effect on survival for breast cancer (hazard ratio (HR) 5 0.88, 95% confidence interval (95% CI) 5 0.81 to 0.96) and prostate cancer (HR 5 0.82, 95% CI 5 0.75 to 0.90). In contrast, family history of cancer was associated with worse survival for nervous system cancers (HR 5 1.24, 95% CI 5 1.05 to 1.47) and ovarian cancer (HR 5 1.20, 95% CI 5 1.01 to 1.43). Furthermore, the poorer survival for ovarian cancer was consistent with a higher FIGO stage and a greater proportion of more aggressive tumors of the serous type. The better survival for patients with a family history of breast and prostate cancer may be due to medical surveillance of family members. The poor survival for ovarian cancer patients with an affected mother or sister is multifactorial, suggesting that these cancers are more aggressive than their sporadic counterparts.

BackgroundA positive association between birth weight (BW) and body mass index (BMI) has been shown among children in many populations. The aim of this study was to investigate BMI trajectory according to BW status and the protective effect of breastfeeding on the prevalence of overweight/obesity in children 6 years of age.MethodsA retrospective cohort study was conducted between January 1, 2008 and December 31, 2016 utilizing data from the National Health Information Database of Korea. The 38,049 subjects were followed until the end of 2016, providing that subjects were completely eligible for all health check-ups from birth to 6 years of age. At each check-up period, multiple logistic regressions were used to investigate the association between BW status (low birth weight [LBW], normal birth weight [NBW], high birth weight [HBW]) and growth development.ResultsHBW infants were highly likely to be overweight/obese compared to NBW infants (odds ratio [OR], 1.70–2.35) and LBW infants were highly likely to be underweight (OR, 1.69–2.20) through 6 years of age. The risk of overweight/obesity decreased significantly if HBW infants were breast-fed for 6 months (OR, 0.54–0.76).ConclusionHBW status is associated with overweight/obesity during early childhood. Exclusive breastfeeding is a significant protective factor against overweight/obesity in children with HBW.

Few birth cohort studies have examined the role of traffic-related air pollution (TRAP) in the development of infantile atopic dermatitis (AD), but none have investigated the role of preventive factors such as green spaces. The aim of this study was to investigate whether exposure to nitrogen dioxide (NO2) and particulate matter with an aerodynamic diameter of <10 μm (PM10) during pregnancy is associated with increased risk of development of AD in 6-month-old children and also to examine how this association changes with residential green space. This study used prospective data from 659 participants of the Mothers and Children’s Environmental Health study. Subjects were geocoded to their residential addresses and matched with air pollution data modeled using land-use regression. Information on infantile AD was obtained by using a questionnaire administered to the parents or guardians of the children. The association between infantile AD and exposure to NO2 and PM10 was determined using logistic regression models. We assessed the effects of residential green spaces using stratified analyses and by entering product terms into the logistic regression models. The risk of infantile AD significantly increased with an increase in air pollution exposure during the first trimester of pregnancy. The adjusted odds ratio (OR) and 95% confidence interval (CI) were 1.219 (1.023–1.452) per 10 μg/m3 increase in PM10 and 1.353 (1.027–1.782) per 10 ppb increase in NO2. An increase in the green space within 200 m of residence was associated with a decreased risk of AD (OR = 0.996, 95% CI: 0.993–0.999). The stratified analysis of residential green space revealed stronger associations between infantile AD and PM10 and NO2 exposure during the first trimester in the areas in the lower tertiles of green space. This study indicated that exposure to TRAP during the first trimester of pregnancy is associated with infantile AD. Less residential green space may intensify the association between TRAP exposure and infantile AD.

Background and AimsHepatocellular carcinoma (HCC) risk in chronic hepatitis B (CHB) substantially decreased in the era of potent antiviral therapy. We developed an optimized HCC risk prediction model for CHB with well‐controlled viremia by nucelos(t)ide analogs (NUCs).MethodWe analysed those who achieved virological response (VR; serum HBV‐DNA < 2000 IU/mL on two consecutive assessments) by NUCs. Liver stiffness by transient elastography, ultrasonography and laboratory tests was performed at the time of confirmed VR. Patients with decompensated cirrhosis or HCC at baseline were excluded. Multivariate Cox‐regression analysis was used to determine key variables to construct a novel risk‐scoring model.ResultsAmong 1511 patients, 9.5% developed HCC. Cirrhosis on ultrasonography (adjusted HR [aHR] 2.47), age (aHR 1.04), male (aHR 1.90), platelet count <135 000/uL (aHR 1.57), albumin <4.5 g/dL (aHR 1.77) and liver stiffness ≥11 kPa (aHR 6.09) were independently associated with HCC. Using these, CAMPAS model was developed with c‐index of 0.874. The predicted and observed HCC probabilities were calibrated with a reliable agreement. Such results were reproduced from internal validation and external validation among the independent cohort (n = 252). The intermediate‐risk (CAMPAS model score 75 ~ 161) and high‐risk (score >161) groups were more likely to develop HCC compared with the low‐risk group (score ≤75) with statistical significances (HRs; 4.43 and 47.693 respectively; both P < .001).ConclusionCAMPAS model derived through comprehensive clinical evaluation of liver disease allowed the more delicate HCC prediction for CHB patients with well‐controlled viremia by NUCs.