Background: Air pollutants are considered as non-negligible risk factors of idiopathic pulmonary fibrosis (IPF). However, the relationship between long-term air pollution and the incidence of IPF is unknown. Our objective was to explore the associations of air pollutants with IPF risk and further assess the modification effect of genetic susceptibility.Methods: We used land-use regression model estimated concentrations of nitrogen dioxide (NO₂), nitrogen oxides (NO_x) and particulate matter (fine particulate matter with diameter <2.5 μm (PM_2.5) and particulate matter with diameter <10 μm (PM₁₀)). The polygenic risk score (PRS) was constructed using 13 independent single nucleotide polymorphisms. Cox proportional hazard models were used to evaluate the associations of air pollutants with IPF risk and further investigate the modification effect of genetic susceptibility. Additionally, absolute risk was calculated.Results: Among 433 738 participants from the UK Biobank, the incidence of IPF was 27.45 per 100 000 person-years during a median follow-up of 11.78 years. The adjusted hazard ratios of IPF for each interquartile range increase in NO₂, NO_xand PM_2.5were 1.11 (95% CI 1.03–1.19), 1.07 (95% CI 1.01–1.13) and 1.09 (95% CI 1.02–1.17), respectively. PM_2.5had the highest population attribution risk, followed by NO_xand NO₂. There were additive interactions between NO₂, NO_xand PM_2.5and genetic susceptibility. Participants with a high PRS and high air pollution had the highest risk of incident IPF compared with those with a low PRS and low air pollution (adjusted hazard ratio: NO₂3.94 (95% CI 2.77–5.60), NO_x3.08 (95% CI 2.21–4.27), PM_2.53.65 (95% CI 2.60–5.13) and PM₁₀3.23 (95% CI 2.32–4.50)).Conclusion: Long-term exposures to air pollutants may elevate the risk of incident IPF. There are additive effects of air pollutants and genetic susceptibility on IPF risk.

Prenatal exposure to thallium is related to adverse birth outcomes. However, little is known about the effects of prenatal exposure to thallium on the mitochondrial DNA copy number (mtDNAcn) in newborns; such knowledge might reveal a potential mechanism linking maternal thallium exposure and adverse birth outcomes. To investigate the trimester-specific associations of maternal thallium exposure with cord blood leukocyte mtDNAcn. A total of 746 pregnant women with trimester-specific urinary samples and cord blood samples were recruited from Wuhan Children Hospital between November 2013 and March 2015 in Wuhan City, China. The concentration of thallium in maternal urine was quantified using inductively coupled plasma mass spectrometry (ICP-MS). Cord blood leukocyte mtDNAcn was measured by real-time quantitative polymerase chain reaction (qPCR). Trimester-specific associations of specific gravity (SG)-adjusted urinary thallium concentrations with mtDNAcn were estimated using a multiple informant model. The geometric mean value of maternal urinary thallium was 0.34 μg/L, 0.36 μg/L, and 0.34 μg/L for the first, second, and third trimesters, respectively. Prenatal exposure to thallium during the first trimester, rather than during the second or the third trimester, was identified as negatively related to mtDNAcn. The multiple informant model showed a 10.4% lower level of mtDNAcn with each doubling increase of thallium levels (95% CI, -16.4%, -3.9%; P = 0.002). The observed associations were stronger among female newborns and among newborns born to older mothers. The present study revealed a significant negative association between maternal thallium exposure during early pregnancy and cord blood leukocyte mtDNAcn in Chinese newborns, pointing to the important role of mitochondria as a target of thallium toxicity in early pregnancy.

Telomere length (TL) is considered as a surrogate of biological aging and has been related to aging-related diseases. The initial setting of newborn TL has important implications for telomere dynamics in adulthood, and is affected by the intrauterine environment. However, the effects of prenatal air pollution exposure on the initial setting of newborn TL are poor understood. We aimed to explore the trimester-specific relationships between maternal air pollution exposure and newborn TL. Between November 2013 and March 2015, a total of 762 mother-newborn pairs were recruited in a birth cohort study in Wuhan, China. Relative cord blood TL was assessed using quantitative real-time polymerase chain reaction. Maternal exposures to PM2.5, PM10, SO2, CO, and NO2, were determined using spatial-temporal land use regression models. Multiple informant models were applied to explore the trimester-specific associations of maternal air pollution exposure with cord blood TL. In single-pollutant models, a 10 μg/m3 increase in PM2.5, PM10, SO2, and a 100 μg/m3 increase in CO during the third trimester were related to 3.71% (95% confidence interval [CI]: -6.06%, -1.30%), 3.24% (95% CI: -5.29%, -1.14%), 11.07% (95% CI: -18.86%, -2.53%), and 3.67% (95% CI: -6.27%, -1.00%) shorter cord blood TL, respectively. The inverse relationships between exposures to PM2.5, PM10, SO2, and CO during the third trimester and cord blood TL were more evident in male infants. In multi-pollutant models, exposures to PM2.5 and PM10 during the third trimester were both related to shorter cord blood TL, but not SO2 and CO. This study suggested that maternal exposures to PM2.5, PM10, CO, and SO2 during the third trimester were related to shorter newborn TL, which highlights the importance of improving air quality in favor of subsequent health in later life of newborns.

Newborn telomere length (TL) is considered a potential marker for future disease and lifelong health, but few epidemiological studies have examined the determinants of TL in early life. The study aim was to investigate whether there is an association between prenatal cadmium exposure and relative cord blood TL in Chinese newborns. Participants were 410 mother–newborn pairs drawn from a prospective birth cohort study conducted in Wuhan, China, between November 2013 and March 2015. Urine samples were collected from pregnant women during their period of institutional delivery. Urinary cadmium concentrations were measured by inductively coupled plasma mass spectrometry. The real-time quantitative polymerase chain reaction detection was used to measure relative TL using genomic DNA isolated from umbilical cord blood leukocytes. Multivariate linear regression models were used to estimate the effect of prenatal urinary cadmium concentration on relative cord blood TL. The geometric mean of maternal urinary cadmium concentration was 0.68 μg/g creatinine. In the multivariate-adjusted linear regression model, per doubling of maternal urinary cadmium concentration was associated with 6.83% (95% CI − 11.44%, − 1.97%; P = 0.006) shorter relative cord blood TL. Stratified analyses indicated that the inverse association between prenatal urinary cadmium and newborn relative TL was more pronounced among female infants and mothers < 29 years, while there were no significant effect modification according to infant sex (P for interaction = 0.907) and maternal age (P for interaction = 0.797). The findings indicated that increased maternal urinary cadmium was associated with shortened relative cord blood TL. The results provide more evidence of the negative effects of environmental cadmium exposure and suggest that accelerated aging or cadmium-related diseases may begin in early life.

Environmental Health Perspectives is an Open Access journal published by the National Institute of Environmental Health Sciences. Environmental Health Perspectives is an Open Access journal published by the National Institute of Environmental Health Sciences.