Prenatal fine particulate matter (PM₂.₅) exposure has been associated with impaired offspring neurodevelopment; however, the association of PM₂.₅ exposure during preconception with offspring’s neurodevelopment and factors responsible for this association are still unclear. This study estimated the associations of PM₂.₅ exposure during preconception and the first trimester with offspring neurodevelopment and evaluated whether maternal thyroid hormones mediate these associations. We recruited 1329 mother-child pairs between 2013 and 2015 in Wuhan, China. PM₂.₅ exposure levels of each woman during the 3 months preconception and the first trimester were estimated using land-use regression models. Offspring neurodevelopment characterized by mental developmental index (MDI) and psychomotor developmental index (PDI) were measured at 24 months of age. Maternal serum levels of free thyroxine (FT3), free triiodothyronine (FT4), and thyroid-stimulating hormone (TSH) during early pregnancy were measured of a subset of the 1329 women (551 women). Generalized estimation equation and general linear regression models were used to estimate the associations between maternal PM₂.₅ exposure, thyroid hormones, and offspring neurodevelopment. After adjusting for potential confounders, we found that either among all participants or the subset, PM₂.₅ exposure during preconception and the first trimester was negatively associated with offspring PDI. Double increment in the first trimester PM₂.₅ exposure was significantly associated with 3.43 and 6.48 points decrease in offspring MDI. In the subset, each doubling of PM₂.₅ exposure during preconception and the first trimester was significantly associated with 7.93 and 8.02 points decrease in maternal FT4 level, respectively. Increased maternal FT4, in turn, was associated with increased PDI (β = 16.69, 95% CI: 5.39, 27.99). About 7.7% (95% CI: 2.0%–19.4%) and 8.6% (95% CI: 3.0%, 22.1%) of the effect of PM₂.₅ exposure during preconception on offspring PDI was mediated through maternal FT4 and the FT4/FT3 ratio, respectively.

Nitrogen dioxide (NO₂) is a well-established traffic emissions tracer and has been associated with multiple adverse health outcomes. Short- and long-term exposure to NO₂ has been studied and is well-documented in existing literature, but information on intermediate-term NO₂ effects and mortality is lacking, despite biological plausibility. We obtained daily NO₂ and mortality data from 42 counties in China from 2013 to 2015. Distributed-lag non-linear models were employed to investigate the relationship between non-accidental mortality and NO₂ up to 30 days before the event, including PM₂.₅, temperature, relative humidity, and holidays as covariates in a random effects meta-analysis pooling county-specific estimates. We repeated the analysis for cardiovascular- and respiratory-related mortality, and explored sex-stratified associations. Per 10 μg/m³ increase in NO₂, we estimated a 0.13% (95%CI: 0.03, 0.23%), 0.57% (95%CI: −0.04, 1.18%), and −0.14% (95%CI: −1.63, 1.37%) change in non-accidental mortality for same-day and previous-day NO₂ (lag0-1 cumulated), in the preceding 7 days (lag0-7 cumulated), and in the preceding 30 days (lag0-30 cumulated), respectively. The strongest estimate was observed for respiratory-related mortality in the lag0-30 cumulated effect for women (3.12%; 95%CI: −1.66, 8.13%). We observed a trend of higher effect estimates of intermediate-term NO₂ exposure on respiratory mortality compared to that of the short-term, although the differences were not statistically significant. Our results at longer lags for all-cause and cardiovascular mortality were sensitive to modeling choices. Future work should further investigate intermediate-term air pollution exposure given their potential biological relevance, but in larger scale settings.

Manganese (Mn) is an essential trace element, but an excess or accumulation can be toxic. Until now, few studies have examined the effects of maternal Mn level on the risk of spontaneous preterm birth (SPB). The aims of this study were to examine the association between maternal Mn level and the risk of SPB at the early stage of pregnancy, and investigate whether this association was modified by single nucleotide polymorphisms (SNPs) in genes of superoxide dismutase (SOD) and catalase (CAT). We conducted a nested case-control study in three maternal and child health care hospitals in Shanxi province, China, from December 2009 to December 2013. From an overall cohort of 4229 women, 528 were included in our study, including 147 cases of SPB and 381 controls. Maternal blood samples were collected during 4–22 gestational weeks. The maternal serum concentrations of Mn was measured using inductively coupled plasma–mass spectrometry. We found the maternal Mn concentration in the case group (median: 1.55 ng/mL) was significantly higher than that in the control group (median: 1.27 ng/mL). Compared to the lowest level, the SPB risk was significantly increased to 1.44 (95%CI: 0.60–3.43), 2.42 (95%CI: 1.06–5.55) and 2.46 (95%CI: 1.08–5.62) respectively for the second, third and fourth quartiles in first trimester, but not significant in second trimester or overall. When exposure to a high Mn level, women who with AA (6.36, 95%CI: 1.57–25.71) and AG (3.04, 95%CI: 1.59–5.80) of rs2758352, with CC (2.34, 95%CI: 1.31–4.18) of rs699473, and with GG (2.26, 95%CI: 1.22–4.16) of rs769214 were more likely to develop a SPB, but not among women with other genotypes. In conclusion, high maternal serum Mn level is associated with the increased SPB risk in first trimester, and the association is modified by maternal SNPs of SOD2, SOD3 and CAT.

It is likely that pollution from chemical facilities will affect the health of any exposed population; however, the majority of scientific evidence available has focused on occupational exposure rather than environmental. Consequently, this study assessed whether there could have been an excess of cancer-related mortality associated with environmental exposure to pollution from chemical installations – for populations residing in municipalities in the vicinity of chemical industries. To this end, we designed an ecological study which assessed municipal mortality due to 32 types of cancer in the period from 1999 to 2008. The exposure to pollution was estimated using distance from the facilities to the centroid of the municipality as a proxy for exposure. In order to assess any increased cancer mortality risk in municipalities potentially exposed to chemical facilities pollution (situated at a distance of ≤5 km from a chemical installation), we employed Bayesian Hierarchical Poisson Regression Models. This included two Bayesian inference methods: Integrated Nested Laplace Approximations (INLA) and Markov Chain Monte Carlo (MCMC, for validation). The reference category consisted of municipalities beyond the 5 km limit. We found higher mortality risk (relative risk, RR; estimated by INLA, 95% credible interval, 95%CrI) for both sexes for colorectal (RR, 1.09; 95%CrI, 1.05–1.15), gallbladder (1.14; 1.03–1.27), and ovarian cancers (1.10; 1.02–1.20) associated with organic chemical installations. Notably, pleural cancer (2.27; 1.49–3.41) in both sexes was related to fertilizer facilities. Associations were found for women, specifically for ovarian (1.11; 1.01–1.22) and breast cancers (1.06; 1.00–1.13) in the proximity of explosives/pyrotechnics installations; increased breast cancer mortality risk (1.10; 1.03–1.18) was associated with proximity to inorganic chemical installations. The results suggest that environmental exposure to pollutants from some types of chemical facilities may be associated with increased mortality from several different types of cancer.

Humans are exposed to various anthropogenic chemicals in daily life, including endocrine-disrupting chemicals (EDCs). However, there are limited data on chronic, low-level exposure to such contaminants among the general population. Here hair analysis was used to investigate the occurrence of four polychlorinated biphenyls (PCBs), seven polybrominated diphenyl ethers (PBDEs) and two bisphenols (BPs) in 204 Chinese women living in the urban areas of Baoding and Dalian and 311 pregnant French women. All the PCBs and PBDEs tested here were more frequently detected in the hair samples of the French women than in those of the Chinese women. In both cohorts, PCB 180 and BDE 47 were the dominant PCB and PBDE congener, respectively. PCB 180 was found in 82% of the French women and 44% of the Chinese women, while the corresponding values of BDE 47 were 54% and 11%, respectively. A discriminant analysis further demonstrated the difference in PCBs and PBDEs exposure profile between the two cohorts. These results demonstrate that hair analysis is sufficiently sensitive to detect exposure to these pollutants and highlight differences in exposure between populations even at environmental levels. Although BPA and BPS were found in 100% of the hair samples in both cohorts, the French women had significantly higher levels of BPA and BPS than the Chinese women. The median concentrations of BPA were one order of magnitude higher than BPS in both the Chinese (34.9 versus 2.84 pg/mg) and the French women (118 versus 8.01 pg/mg) respectively. Our results suggest that both French and Chinese populations were extensively exposed to BPA and BPS.

Temperature has been associated with population health, but few studies have projected the future temperature-related years of life lost attributable to climate change. To project future temperature-related disease burden in Tianjin, we selected years of life lost (YLL) as the dependent variable to explore YLL attributable to climate change. A generalized linear model (GLM) and distributed lag non-linear model were combined to assess the non-linear and delayed effects of temperature on the YLL of non-accidental mortality. Then, we calculated the YLL changes attributable to future climate scenarios in 2055 and 2090. The relationships of daily mean temperature with the YLL of non-accident mortality were basically U-shaped. Both the daily mean temperature increase on high-temperature days and its drop on low-temperature days caused an increase of YLL and non-accidental deaths. The temperature-related YLL will worsen if future climate change exceeds 2 °C. In addition, the adverse effects of extreme temperature on YLL occurred more quickly than that of the overall temperature. The impact of low temperature was greater than that of high temperature. Men were vulnerable to high temperature compared with women. This analysis highlights that the government should formulate environmental policies to reach the Paris Agreement goal.

Breast cancer is the most frequent tumor in women worldwide, although well-established risk factors account for 53%–55% of cases. Therefore, other risk factors, including environmental exposures, may explain the remaining variation. Our objective was to assess the relationship between risk of breast cancer and residential proximity to industries, according to categories of industrial groups and specific pollutants released, in the context of a population-based multicase-control study of incident cancer carried out in Spain (MCC-Spain). Using the current residence of cases and controls, this study was restricted to small administrative divisions, including both breast cancer cases (452) and controls (1511) in the 10 geographical areas recruiting breast cancer cases. Distances were calculated from the respective woman's residences to the 116 industries located in the study area. We used logistic regression to estimate odds ratios (ORs) and 95% confidence intervals (95%CIs) for categories of distance (between 1 km and 3 km) to industrial plants, adjusting for matching variables and other confounders. Excess risk (OR; 95%CI) of breast cancer was found near industries overall (1.30; 1.00–1.69 at 3 km), particularly organic chemical industry (2.12; 1.20–3.76 at 2.5 km), food/beverage sector (1.87; 1.26–2.78 at 3 km), ceramic (4.71; 1.62–13.66 at 1.5 km), surface treatment with organic solvents (2.00; 1.23–3.24 at 3 km), and surface treatment of plastic and metals (1.51; 1.06–2.14 at 3 km). By pollutants, the excess risk (OR; 95%CI) was detected near industries releasing pesticides (2.09; 1.14–3.82 at 2 km), and dichloromethane (2.09; 1.28–3.40 at 3 km). Our results suggest a possible increased risk of breast cancer in women living near specific industrial plants and support the need for more detailed exposure assessment of certain agents released by these plants.

Organochlorine pesticides (OCPs), including dichlorodiphenyltrichloroethane (DDT) and its metabolites [dichlorodiphenyldichloroethylene (DDE) and dichlorodiphenyldichloroethane], hexachlorocyclohexanes (HCHs), and hexachlorobenzene (HCB), are widely detected in humans despite the considerable decline in environmental concentrations. To understand the placental transfer of OCPs and the possible maternal influence on them, we measured the concentrations of DDTs, HCHs, and HCB in 102 paired samples of maternal and cord sera, and placentas collected in Shanghai, China. The median concentrations of DDTs and HCHs were the highest in maternal sera (601, 188 ng g⁻¹ lipid), followed by umbilical cord sera (389, 131 ng g⁻¹ lipid), and placentas (65, 37 ng g⁻¹ lipid). 4,4′-DDE, β-HCH, and HCB were the predominant contaminants in the three matrices. The ubiquitous existence of OCPs, and the significant concentration relationships of DDTs, HCHs, and OCPs in the three matrices suggested placental transfer from mother to fetus. The lipid-based concentration ratios of 4,4′-DDE, β-HCH, and HCB in umbilical cord serum to those in maternal serum (F/M), and ratios of placenta to maternal serum (P/M) ranged from 0.66 to 1.01, and 0.12 to 0.25, respectively. Maternal variables affected the levels of fetal contamination. For primiparous women, significant correlations between maternal age and maternal HCHs, and between pre-pregnancy body mass index (BMI) and maternal HCHs were found. The negative effect of parity, and the positive effect of food consumption on maternal OCP concentrations were also observed, although there were no significant differences. The possible influence of parity on F/M and P/M of 4,4′-DDE suggested borderline significant differences between primiparous and multiparous women. Also, slight group differences were observed between elder and younger women, and between overweight and normal/underweight women. Parity seems to have a potential influence on transfer ratios of some OCP pollutants.

Thallium (Tl) is a well-recognized hazardous toxic heavy metal that has been reported to have embryotoxicity and fetotoxicity. However, little is known about its association with preterm birth (PTB) in humans. We aimed to evaluate the predictors of Tl exposure and assessed its relation with PTB. The study population included 7173 mother-infant pairs from a birth cohort in Wuhan, China. Predictors of Tl concentrations were explored using linear regression analyses, and associations of Tl exposure with risk of PTB or gestational age at birth were estimated using logistic regression or generalized linear models. The geometric mean and median values of urinary Tl concentrations were 0.28 μg/L (0.55 μg/g creatinine) and 0.29 μg/L (0.53 μg/g creatinine). We found that maternal urinary Tl concentrations varied by gestational weight gain, educational attainment, multivitamin and iron supplementations. Women with Tl concentrations higher than 0.80 μg/g creatinine were at higher risk of giving birth prematurely versus those with Tl concentrations lower than 0.36 μg/g creatinine [adjusted odds ratio (95% confidence interval (CI)): 1.55 (1.05, 2.27)], and the association was more pronounced in PTB with premature rupture of membranes (PROM) rather than in PTB without PROM. About 3-fold increase in creatinine-corrected Tl concentrations were associated with 0.99-day decrease in gestational length (95% CI: −1.36, −0.63). This is the first report on the associations between maternal Tl exposure and the risk of PTB.