The objective of this study was to conduct a systematic review to provide summarized evidence on the association between maternal exposure to particulate air pollution and birth weight (BW) and preterm birth (PTB) after taking into consideration the potential confounding effect of maternal smoking. We systematically searched all published cohort and case-control studies examining BW and PTB association with particulate matter (PM, less than or equal to 2.5μm and 10.0 μm in diameter, PM2.5 and PM10, respectively) from PubMed and Web of Science, from January 1980 to April 2015. We extracted coefficients for continuous BW and odds ratio (OR) for PTB from each individual study, and meta-analysis was used to combine the coefficient and OR of individual studies. The methodological quality of individual study was assessed using a standard protocol proposed by Downs and Black. Forty-four studies met the inclusion criteria. In random effects meta-analyses, BW as a continuous outcome was negativelyassociated with 10 μg/m(3) increase in PM10 (-10.31 g; 95% confidence interval [CI], -13.57 to -3.13 g; I-squared=0%, p=0.947) and PM2.5 (-22.17 g; 95% CI, -37.93 to -6.41 g; I-squared=92.3%, p <0.001) exposure during entire pregnancy, adjusted for maternal smoking. A significantly increased risk of PTB per 10 μg/m(3) increase in PM10 (OR, 1.23; 95% CI, 1.04 to 1.41; I-squared=0%, p =0.977) and PM2.5 (OR, 1.14; 95% CI, 1.06 to 1.22; I-squared=92.5%, p <0.001) exposure during entire pregnancy was observed. Effect size of change in BW per 10 μg/m(3) increase in PM tended to report stronger associations after adjustment for maternal smoking. While this systematic review supports an adverse impact of maternal exposure to particulate air pollution on birth outcomes, variation in effects by exposure period and sources of heterogeneity between studies should be further explored.

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: Patients with chronic obstructive pulmonary disease (COPD) have an increased risk of developing lung cancer. Some studies have also suggested that diabetes mellitus (DM) may increase the risk of developing lung cancer. This study aimed to investigate whether type 2 DM (T2DM) is associated with an increased risk of lung cancer in patients with COPD.Materials and methods: We conducted a retrospective analysis on two cohorts: the National Health Insurance Service-National Sample Cohort (NHIS-NSC) of Korea and the Common Data Model (CDM) database of a university hospital. Among patients newly diagnosed with COPD in each cohort, those with a lung cancer diagnosis were included, and a control group was selected through propensity score matching. We used the Kaplan–Meier analysis and Cox proportional hazard models to compare lung cancer incidence between patients with COPD and T2DM and those without T2DM.Results: In the NHIS-NSC and CDM cohorts, we enrolled 3,474 and 858 patients with COPD, respectively. In both cohorts, T2DM was associated with an increased risk of lung cancer [NHIS-NSC: adjusted hazard ratio (aHR), 1.20; 95% confidence interval (CI), 1.02–1.41; and CDM: aHR, 1.45; 95% CI, 1.02–2.07). Furthermore, in the NHIS-NSC, among patients with COPD and T2DM, the risk of lung cancer was higher in current smokers than in never-smokers (aHR, 1.45; 95% CI, 1.09–1.91); in smokers with ≥30 pack-years than in never-smokers (aHR, 1.82; 95% CI, 1.49–2.25); and in rural residents than in metropolitan residents (aHR, 1.33; 95% CI, 1.06–1.68).Conclusion: Our findings suggest that patients with COPD and T2DM may have an increased risk of developing lung cancer compared to those without T2DM.

Background/Objectives: Prescribing inhaled corticosteroids (ICS) to patients with bronchiectasis may be controversial. Studies investigating the association between ICS and the risk of lung cancer in patients with bronchiectasis are rare. Methods: Patients with bronchiectasis were enrolled from the National Sample Cohort Data of the National Health Insurance Service (NHIS-NSC) in Korea. Among them, patients with lung cancer were selected as the case group, and the control group was selected by matching the patient group with the propensity score at 1:5 for age, sex, and recruitment year. Kaplan–Meier analysis and Cox proportional hazards model analysis were performed to determine the risk of lung cancer associated with ICS use in patients with bronchiectasis. In addition, ICS dose–response analysis was performed to determine the risk of lung cancer in patients with bronchiectasis. Results: A total of 19,043 patients with bronchiectasis were included in the study. In patients with bronchiectasis, ICS use was associated with an increased risk of lung cancer. After adjusting for age, sex, pack-years of smoking, body mass index (BMI), household income, region of residence, and Charlson comorbidity index (CCI), ICS use was found to be significantly associated with an increased risk of lung cancer (aHR 1.40, 95% CI 1.17 to 1.67). Furthermore, we found that the cumulative incidence of lung cancer increased with the cumulative dose of ICS in patients with bronchiectasis. Subgroup analysis of lung cancer risk in patients with bronchiectasis using ICS showed that the risk of lung cancer was significantly higher in those aged 70 years or older, male, with a BMI of 23 kg/m² or higher, with a history of smoking, with a higher number of pack-years of smoking, and with a higher CCI. Conclusions: In patients with bronchiectasis, the use of ICS is associated with an increased risk of lung cancer, which is affected by the cumulative dose of ICS.