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Fine particulate matter (PMA total of 298,069 participants from the UK Biobank study without lung cancer at baseline were included in this study. Hazard ratios (HRs) with 95 % confidence intervals (CIs) were estimated using multivariable Cox proportional models for the association of lung cancer and its subtypes with PMDuring 10.4 years of follow-up, 1683 incident lung cancer cases were identified. Our analysis found that genetic variants, smoking, and PMGenetic susceptibility, smoking, and PM

Studies on the obesogenic effect of air pollution on children have been mixed and sparse. Moreover, due to insufficient air monitoring, few studies have investigated the role of more tiny but unregulated particles (ambient particles with a diameter of 0.1 μm or less, ultrafine particles).We sought to explore the associations between long-term exposure to ambient ultrafine particles (UFPs) and childhood obesity in Chinese children.In this cross-sectional study, we randomly recruited 47,990 children, aged 6-18 years, from seven cities in Northeastern China between 2012 and 2013. Child age- and sex-specific z-scores for body mass index (BMI Z-score) and weight status were generated using the World Health Organization growth reference. Four-year average concentrations of UFPs and airborne particulates of diameter ≤ 1 μm (PMWe found that UFPs exposure was associated with greater childhood BMI Z-score and a higher likelihood of obesity. Compared with the lowest quartile, higher quartiles of UFPs were associated with greater odds for obesity prevalence in children (i.e., the adjusted OR was 1.25; 95 % CI, 1.12-1.39; 1.43; 95 % CI, 1.27-1.61; and 1.41; 95 % CI, 1.25-1.58 for the second, third, and fourth quartile, respectively). Similar associations were observed for PMLong-term UFPs exposure was associated with a greater likelihood of childhood obesity, and stronger associations on BMI Z-score were observed in boys and children living close to roadways. This study indicates that more attention should be paid to the health effects of UFPs, and routinely monitoring of UFPs should be considered.

Background Ambient air pollutant directly contacts with the eyes, however, the effect of ambient fine particulate matter (PM2.5) and ozone (O3) on vision impairment, such as presbyopia, has been kept largely unknown. Methods We surveyed a total of 36,620 participants aged 50 years and above in six low- and middle-income countries. Ambient annual concentrations of PM2.5 and O3 for the residential community were estimated using satellite data and chemical transport model. A mixed effects model was utilized to assess the effects of ambient PM2.5 and O3 on presbyopia, as well as their combined effects. Results A total of 13,841 presbyopia cases were identified among the participants with a prevalence rate of 41.17%. For both PM2.5 and O3, we found a J-shaped exposure-response relationship with the threshold being identified at 15 μg/m3 for PM2.5 and 55 μg/m3 for O3. The odds ratio (OR) of presbyopia was 1.15 (95% CI: 1.09, 1.21) for each 10 μg/m3 increase in PM2.5 above 15 μg/m3 and 1.37 (95% CI: 1.23, 1.54) for O3 above 55 μg/m3 after adjusting for various potential confounding factors. There appeared to be a synergistic interaction between ambient PM2.5 and O3 on presbyopia in the additive model, the combined effect was significantly larger than the sum of their individual effects, with a synergistic index of 2.39. Conclusion This study supports that exposures to ambient PM2.5 and O3 might be important risk factors of presbyopia among old adults, and simultaneously exposure to high level of the two pollutants could intensify their individual effects.

Ambient air pollution has been widely associated with increased mortality and years of life lost (YLL) from various diseases. However, no study has assessed that the effects of air pollution on overall YLL were due to increased number of mortalities or average YLL per death.We first conducted a time-series study from 2013 to 2016, covering six Chinese megacities. Generalized additive models with a Gaussian link were utilized to estimate the associations of fine particulate matter (PMA total of 1,586,741 deaths from non-accidental causes and 21,916,857 YLLs were recorded in the six cities, providing an average of 13.81 daily YLLs per death. Significant effects of PMOur study indicates observed associations between air pollution and YLL might be mainly induced by increasing mortality count, rather than increasing average life lost for each death. More relevant intervention should be performed to reduce the number of deaths due to air pollution.

Cohort evidence that links long-term exposures to air pollution and mortality comes largely from the United States and European countries. We investigated the relationship between long-term exposures to particulate matter

Background Little is known about whether exposure to pets influences the association between hypertension and environmental tobacco smoke (ETS). The current study aims to examine the interaction of pet ownership on ETS exposure and the development of hypertension in children. Methods From 2012 to 2013, a total of 9354 children, 5 to 17 years of age, were recruited from 62 schools in seven northeastern cities. BP in children was measured and hypertension was defined as an average diastolic blood pressure (DBP) or systolic blood pressure (SBP) at or above the 95th percentile for that child's age, sex, and height. Pet ownership in three different time periods (in utero, past 2 years, and currently) and ETS exposure data were collected from parents via a questionnaire. Two-level regressions were used for the data analyses. Results The data show consistent, significant interactions between exposure to pets and effects from ETS. Children who were not exposed to pets experienced stronger effects from ETS on hypertension when compared to those exposed to pets, and the protective effect of pet ownership became stronger with a greater number of pets in the home. Exposure to in utero ETS was associated with hypertension [adjusted odds ratio (aOR) = 1.32, 95% confidence interval (CI): 1.13–1.54] only for those children without pet exposure in utero but not for those with pets (aOR = 0.75; 95% CI: 0.49–1.15) (pinteraction Conclusion This study indicates an inverse relationship between pet ownership and ETS, potentially pointing to pet ownership as protecting against the development of hypertension in children.

Objectives Prenatal exposure to air pollutant has been associated with congenital heart defect (CHD). However, no study has investigated this effect in pre-pregnancy overweighted women. This study aimed to evaluate gestational exposure to particulate pollutant (PM2.5) and gaseous air pollutants (O3 and NO2) on the risk of CHD, and explore the potential effect modifiers including maternal age, pre-pregnancy BMI and pregestational diseases. Methods In this birth cohort study, a total of 63,213 pregnant women in Foshan, China were initially recruited and followed from their first hospital visit for pregnancy to delivery during 2015–2019. CHD cases were confirmed by the records in hospital- and population- based birth defect surveillance systems. Air pollutant exposures were estimated by the daily concentrations measured in air monitoring stations in each participant's residential county. Mixed-effects regression models, adjusted for potential confounding factors were applied to estimate the associations between air pollutant and CHD during the first three months of the pregnancy. Results A total of 985 (1.6%) newborns were identified as CHD cases. For each 10 μg/m3 increase in ambient O3 during the 1st month, the OR values for CHD were 1.03 (95% CI: 0.94, 1.13) in pre-pregnancy normal weighted women and 1.24 (95% CI: 1.01, 1.53) in pre-pregnancy overweighted women. For each 10 μg/m3 increase in NO2 during the 3rd month, the OR values for CHD were 1.09 (95% CI: 1.01, 1.18) in pre-pregnancy normal weighted women and 1.27 (95% CI: 1.07, 1.51) in pre-pregnancy overweighted women. No significant associations were found between PM2.5 exposure and CHD in our analysis. Conclusions This study demonstrates that gaseous air pollutants (O3 and NO2) exposure during the cardiac embryogenesis period is associated with an increased risk of CHD, particularly for pre-pregnancy overweighted women.

Perfluoroalkyl and polyfluoroalkyl substances (PFASs), as well as polymers of PFASs, have been widely used in commercial applications and have been detected in humans and the environment. Previous epidemiological studies have shown associations between particular PFAS chemicals and serum lipid concentrations in adults, particularly perfluorooctane sulfonic acid (PFOS) and perfluorooctanoic acid (PFOA). There exists, however, limited information concerning the effect of PFASs have on serum lipids among children. In the present cross-sectional study, 225 Taiwanese children (12-15 years of age) were recruited to determine the relationship between serum level PFASs and lipid concentration. Results showed that eight out of ten particular PFASs were detected in the serum of >94% of the participants. Serum PFOS and perfluorotetradecanoic acid (PFTA) levels were at an order of magnitude higher than the other PFASs, with arithmetical means of 32.4 and 30.7 ng/ml in boys and 34.2 and 27.4 ng/ml in girls, respectively. However, the variation in serum PFTA concentration was quite large. Following covariate adjustment, linear regression models revealed that PFOS, PFOA, and perfluorononanoic acid (PFNA) were positively associated with total cholesterol (TC), low-density lipoprotein (LDL) and triglycerides (TG), particularly for PFOS and PFTA. Quartile analysis, with the lowest exposure quartile as a reference, yielded associations between serum PFTA and elevations in TC (p=0.002) and LDL (p=0.004). Though not statistically significant, high-density lipoprotein (HDL) appeared to decrease linearly across quartiles for PFOS and PFOA exposure. In conclusion, a significant association was observed between serum PFASs and lipid level in Taiwanese children. These findings for PFTA are novel, and emphasize the need to investigate the exposure route and toxicological evidence of PFASs beyond PFOS and PFOA.