Environmental Health最新文献

Objective: Children gradually develop motor skills that enable them to move efficiently in various daily activities such as self-care, academics and sports. The impact of prenatal exposure to endocrine disruptors (EDCs) on these performances remains understudied and current results are inconsistent. This study aims at examining the neuromotor function of Belgian preschoolers exposed in utero to a mixture of some of these chemicals.

Methods: From 2014 to 2016, 66 children (35 boys and 31 girls) were recruited for a longitudinal cohort study. Two polychlorinated biphenyls (PCBs) and four perfluoroalkyl substances (PFASs) were measured in cord serum. A standardized motor evaluation, the Movement Assessment Battery for Children II (MABC-II), and a clinical sensori-motor assessment examining minor neurological dysfunction were administered at 6 years of age. The impact of the mixture of EDCs on neuromotor outcome measures was evaluated using two validated statistical models. Sex-specific analyses were also conducted.

Results: Using a principal component analysis, a negative association was identified between a mixture of PCB-153 and - 180 and the Total Clinical examination score in the whole population (β (95% CI) = -15.8 (-26.51; -5.09), p = 0.005). After stratification by sex, negative associations were observed between the Gross Motor score of the MABC-II test and prenatal exposure to a mixture of PFASs and PCB-180, specifically in boys. This association was consistent across both the weighted quantile sum regression model (β (95% CI) = -2.36 (-3.42; -0.62), p = 0.023) and the principal component approach (β (95% CI) = -1.09 (-2.15; -0.13), p = 0.044).

Conclusion: Our findings suggest that the neuromotor function of young children is adversely influenced by prenatal exposure to toxicants in a sex-specific manner.

Extensive use of per- and polyfluoroalkyl substances (PFAS) has resulted in their ubiquitous presence in human blood. PFAS exposures have been associated with multiple adverse human health effects. Biomonitoring studies have focused on long-chain PFASs, but these are being replaced by short-chain PFASs or with alternate PFAS chemistries (or replacement chemistries such as GenX), resulting in changes in human exposures with time. Here, we take advantage of serum samples collected as part of a clinical trial testing the efficacy of a dietary fiber intervention to reduce serum cholesterol to investigate exposure to PFASs in Canadian participants. Serum samples were collected from 72 participants (adult males with elevated cholesterol) in 2019-2020 at baseline and after 4 weeks of the intervention and were analyzed for 17 PFASs. The highest geometric mean serum concentrations of PFAS measured at baseline corresponded to PFOSA (7.1 ng/ml), PFOS (4.2, ng/ml), PFOA (1.8 ng/ml) and PFHxS (1.3 ng/ml). Four long-chain PFASs (PFOA, PFOS, PFOSA and PFHxS) and two short-chain PFASs (PFBA, PFHxA) were detected in 100% of participants. GenX was detected in 71% of participants. Analyses of associations between serum-PFAS concentrations and biomarkers of adverse health outcomes showed the PFBA, PFHxA, PFDA and PFOSA were associated with higher serum gamma-glutamyl transferase concentrations but not with measures of serum-total or low-density lipoprotein cholesterol. Comparison of PFAS concentrations at baseline and after a 4-week follow-up showed that the total PFAS detected decreased in both the control and cholesterol intervention groups. However, the suite of long-chain PFASs of concern identified by the United States National Academies of Sciences, Engineering, and Medicine, significantly decreased only in the cholesterol intervention group. This observation suggests that a sustained dietary fiber intervention may reduce long-chain PFAS body burden, but future intervention studies need to control for PFAS exposure sources and extend the dietary supplement intake beyond 4 weeks. Overall, the results show that exposures to short-chain and replacement chemistry PFASs are common in this Canadian population.

Aims: The study aimed to investigate the association between domestic water hardness and the incidence of AF and the interaction effects between water hardness and genetic susceptibility to incident AF risk. As a secondary objective, its associations with incident heart failure (HF), coronary heart disease (CHD), and stroke were measured.

Methods: The UK Biobank is a prospective cohort study comprising over 500,000 participants recruited in the United Kingdom between 2006 and 2010, aged 37 to 73 years. A total of 447,950 participants did not have prevalent AF, and 423,946 participants who were free of HF, CHD, and stroke at baseline were included. Water hardness was assessed by CaCO₃ concentration. The genetic risk score for AF was based on the standard polygenic risk score. Cox proportional hazards regression models and restricted cubic spline (RCS) analysis were conducted.

Results: During a median follow-up of 13.74 years, 30,726 (6.86%) individuals were diagnosed with AF for the first time. Compared with those with water hardness ≤ 60 mg/L, individuals with domestic water hardness 121-180 mg/L had a 17% lower risk of developing AF (HR 0.83, 95% CI 0.79-0.87), but water hardness of 61-120 mg/L and > 180 mg/L was associated with a higher risk of incident AF (both 1.04, 1.01-1.07). A non-linear relationship between water hardness and incident AF (P for non-linear = 0.001) was found. Individuals with water hardness 121-180 mg/L were also significantly associated with a lower risk of incident HF (HR 0.82, 95% CI 0.75-0.89), CHD (HR 0.80, 95% CI 0.76-0.84) and stroke (HR 0.88, 95% CI 0.81-0.95). There were no significant interaction effects between water hardness level and genetic susceptibility to AF, HF, CHD, and stroke risk (all P for interaction > 0.05).

Conclusion: Potential U-shaped associations between domestic water hardness and incident AF across varying levels of genetic risk were found. Hard water (121-180 mg/L) may offer the most benefits compared to soft water when considering overall cardiovascular health, including AF, HF, CHD, and stroke.

Extreme drought events can impact human health, notably triggering epidemics that impose significant global health and economic burdens. Understanding these effects and developing response strategies is crucial. However, there is limited epidemiological evidence on how climate change influenced ancient epidemics before large-scale urbanization and frequent population movements. In this study, we utilized the Reconstructed East Asian Climate Historical Encoded Series (REACHES) climate database and the self-constructed ancient Chinese epidemics database to examine extreme drought events in ancient China from 1784-1787 CE. We analyzed factors like grain prices, population density, and socioeconomic conditions to explore the temporal and spatial mechanism and influence the degree of extreme drought events on epidemics outbreaks. The results show that there is a clear positive link between drought and the spread of epidemics, with a notable one-year lag effect of drought. Drought impacts epidemics directly and indirectly through locust plague, famine, crop failure, and social turmoil, with famine being the most crucial factor. Official disaster management can mitigate epidemics. This study intuitively shows the relationship between extreme drought events and epidemics in ancient China and offering insights into the climate change-epidemic relationship. Placing the conclusions of this paper in a broader context has global implications, providing historical experience for polycrisis and modern challenges.

Background: Incidence of childhood Ewing sarcoma, a rare cancer affecting bones and soft tissues, is increasing. Environmental exposures during the perinatal period, like air pollution, may play a role. We examined exposure to perinatal ambient fine particulate matter (PM_2.5) and childhood Ewing sarcoma risk in a case-control linkage study nested within a California birth cohort.

Methods: The study included 388 children born in California (1982-2015) and diagnosed with Ewing sarcoma at age 0-19 years (1988-2015), and 19,341 California-born cancer-free controls frequency-matched to cases on birth year (50:1 ratio). Ambient PM_2.5 concentrations at the maternal residence were averaged separately over two time periods, gestation and the first year after birth, using a validated ensemble-based model (categorized as quartiles). We estimated odds ratios (ORs) and 95% confidence intervals (CIs) for the association between perinatal PM_2.5 exposure and Ewing sarcoma risk, adjusting for sex, birth year, race, ethnicity, birth weight, and maternal education and stratifying by Hispanic ethnicity to assess potential disparities in PM_2.5-related cancer risk.

Results: In the overall population, perinatal ambient PM_2.5 exposure was not associated with Ewing sarcoma risk when considering exposure during gestation or the year after birth. Among Hispanic children, who experienced greater air pollution exposure compared to non-Hispanic children, higher PM_2.5 levels during gestation yielded elevated odds of Ewing sarcoma compared to the first quartile (Q2 OR [95% CI] = 1.53 [0.94-2.51]; Q3 = 1.56 [0.95-2.56]; Q4 = 1.39 [0.79-2.47]). Hispanic children also experienced elevated risk in relation to exposure during the year after birth.

Conclusion: Our results provide new suggestive evidence that ambient PM_2.5 may contribute to Ewing sarcoma risk, although these findings were not statistically significant and were specific to Hispanic children. These findings require replication and underscore the need to further evaluate the potential role of ethnicity in the PM_2.5-cancer relationship with genetic ancestry measures and through the lens of environmental justice.

Background: Elevated homocysteine (Hcy) is a pathogenic mechanism of adverse pregnancy outcomes and PM_2.5-induced cardiovascular diseases. We investigated the associations of fine particulate matter (PM_2.5) and chemical constituent exposures with maternal circulatory Hcy in early pregnancy.

Methods: Serum Hcy and 5-methyltetrahydrofolate in 324 women with pregnancy (162 normal early pregnancy [NEP] and 162 early pregnancy loss [EPL]) were measured by ultra-performance liquid chromatography-tandem triple quadrupole mass spectrometry. Daily exposures to PM_2.5 and constituents (black carbon [BC], organic matter, nitrate, ammonium, and sulfate) were accessed using data of Tracking Air Pollution in China platform. Nonlinear and linear associations of average pollutant exposures during the post-conception period with serum Hcy were estimated using generalized additive models and multivariable linear regression models, respectively. Weekly cumulative and distributed lag associations between pollutant exposures within three months before serum collection and Hcy were analyzed by distributed lag nonlinear models combined with multivariable linear regression models. Sensitivity analyses were conducted using constituent residuals instead of constituent concentrations.

Results: Three-month PM_2.5 and the five constituent exposures were associated with elevated serum Hcy in all participants, EPL group, and NEP group, with 3-12 weeks before serum collection being the susceptible exposure time windows. Pollutants-related Hcy were generally higher in EPL group than in NEP group. Higher post-conception PM_2.5, BC, and sulfate exposures increased serum Hcy in lower but not in higher 5-methyltetrahydrofolate subgroup. Sulfate was the highest risk constituent with residual-related increased Hcy. BC residuals of both post-conception and three-month periods increased Hcy in EPL group but not in NEP group.

Conclusions: Maternal circulatory Hcy in early pregnancy increased with PM_2.5 and constituent exposures, with sulfate being the highest risk constituent. BC-related increased Hcy may induce EPL.

Trial registration: The study protocol was registered for clinical trials (ChiCTR1900028619) on December 29, 2019.

Quantifying the impacts of reduction strategies on PM_2.5-bound polycyclic aromatic hydrocarbons (PAHs) is essential for reducing the health risks of PM_2.5. The COVID-19 lockdown provided an opportunity to reveal the quantitative relationship between lockdown measures and the health risks of PAHs. In this study, the characteristics, sources, and health risks of PAHs were investigated during the COVID-19 lockdown in Hohhot. The source-specific health risks of PAHs were assessed using a combination of incremental lifetime cancer risk models (ILCR) and positive matrix factorization (PMF). Compared with the pre-LD period (pre-LD, 87.41 ± 5.98 ng·m^-3), the total concentration of ∑PAHs during the lockdown period (LD, 32.52 ± 2.31 ng·m^-3) decreased by 62.8% in Hohhot. Coal combustion (51.5%), gasoline emissions (21.9%), diesel emissions (12.9%), industrial emissions (9.3%), and biomass burning (4.7%) were the predominant sources of PAHs in Hohhot. Except for male children, the ILCR of all groups exceeded the threshold for high health risks (1 × 10^- 4). Dermal contact is the predominant exposure pathway for carcinogenic risk. Compared with the pre-LD period, the ILCR values decreased by 62.5-62.7% during the LD period. The PMF-ILCR results indicated that industrial emissions (29.1%), coal combustion (28.4%), and diesel emissions (18.5%) were the main sources of ∑ILCR. A Monte Carlo simulation revealed that the cumulative carcinogenic risks at the 95th percentile of the six groups were 1.5-6.3 times the threshold of high health risk (1 × 10^- 4). These results emphasize that regulating industrial emissions and coal combustion is effective in reducing carcinogenic risks in industrial cities with large coal consumption.

Background: Anxiety disorders are a leading cause of severe quality of life impairment and are among the most common mental disorders globally. However, few studies have investigated the association between exposure to high levels of air pollution and an increased risk of developing anxiety disorders. This study aimed to investigate the relationship between air pollutants and hospitalisation for anxiety disorders and the associated economic burden of these hospitalisations in Sichuan, China.

Methods: We collected 7,282 records of anxiety disorder hospitalisation from medical institutions across nine cities between January 1, 2017, and December 31, 2018. Concurrent meteorological and air pollution data, including temperature, humidity, PM_2.5, PM₁₀, SO₂, and CO, were obtained from 183 monitoring stations in Sichuan Province. After controlling for long-term trends, day of the week, and meteorological factors, we employed a time-stratified case-crossover design based on conditional logistic regression to assess the association between concentrations of the four pollutants (PM_2.5, PM₁₀, SO₂, and CO) and hospital admissions for anxiety disorders, with stratified analysis by age, sex, and season. The cost of hospitalisation was evaluated using the cost-of-illness method.

Results: The finding indicated a positive correlation between short-term exposure to air pollutants and hospitalization rates of anxiety disorders. The effect of each 10 µg/m³ increase in airborne particulate matter (PM) and SO₂ on hospital admissions for people with anxiety disorders peaked with a lag of 5 days, and each 1 mg/m³ increase in CO had the greatest effect on the 0-7 day moving average lag, with OR values of PM_2.5:1.002 (95% CI: 1.001,1.004), PM₁₀:1.001 (95% CI: 1.000,1.002), SO₂:1.034 (95% CI: 1.020,1.047), and CO: 1.614 (95% CI: 1.247, 2.089). Air pollution increases the chances of anxiety disorders during the cold season. Furthermore, the elderly are particularly susceptible to these pollutants, which may contribute to an increased hospitalization rates of anxiety disorders (P < 0.05). The total economic cost of hospitalisation for anxiety disorders due to particulate matter pollution was ¥ 966,319 during the study period.

Conclusion: Short-term exposure to PM_2.5, PM₁₀, SO_2, and CO may increase the risk of hospital admissions for anxiety disorders and impose significant financial burdens.

Background: Air pollution is a global public health concern and incidence rates of metabolic syndrome (MetS) are increasing. To evaluate the effect of long-term air pollution exposure, we examined the association between long-term exposure to ambient air pollution and the incidences of MetS among Korean adults.

Methods: We used data from the Korean Genome and Epidemiology Study's Cardiovascular Disease Association Study, a population-based cohort consisting of community-dwelling Korean adults between 2005 and 2011, who were followed up with until 2016 (n = 7,428). Air pollution exposure was estimated using the Congestion Mitigation and Air Quality model based on the participants' addresses. The participants had a physical examination at every visit during follow-up, and MetS was defined based on the National Institute of Health's National Cholesterol Education Program-Adult Treatment Panel III. We used Cox proportional hazard model to analyze the association between long-term air pollution exposure and incidences of MetS per interquartile range (IQR) increment of the annual concentration after adjusting for potential confounders using single and two-pollutant analysis.

Results: The hazard ratios (HR) of MetS per IQR increment in PM_2.5, SO₂, NO₂, and CO were 1.19 (95% CI: 1.12-1.27), 1.57 (95% CI: 1.47-1.68), 1.11 (95% CI: 1.03-1.20), and 1.63 (95% CI: 1.48-1.78), respectively. The incidences of MetS components, which are high blood pressure, elevated fasting glucose, abdominal obesity, high fasting triglyceride (TG), and low fasting high-density lipoprotein (HDL-C), were significantly associated with an IQR increment especially in SO₂ and CO. In subgroup analysis, males had higher risk of MetS than females. The HR was the highest in the 60-69 year old age group for all pollutants.

Conclusion: In the present study, we found that long-term ambient air pollution exposure increased the incidences of MetS and its components among Korean adults, especially in males and the elderly population.

DNA methylation is a critical step in brain development, 5-Methyl-2'-deoxycytidine (5mdC) is one of the global DNA methylation markers. Arsenic and lead exposures have been associated with neurotoxicity, which may be linked to epigenetic changes. Our research sought to investigate the correlation between 5mdC and developmental delay (DD) among preschoolers. Additionally, we assessed whether 5mdC modified the impacts of blood lead and total urinary arsenic levels on DD. We analyzed the concentrations of 5mdC, blood cadmium and lead, and total urinary arsenic in 174 children with DD and 88 healthy children. Global DNA methylation levels are expressed as the ratio 5mdC/2'-dexyguanosine (dG), called 5mdC (%). In our findings, elevated levels of blood lead and total urinary arsenic were significantly associated with DD risk among preschoolers. Furthermore, high 5mdC (%) was related with reduced risk of DD, with an odds ratio (OR) and 95% confidence interval (CI) of 0.14 (0.06 - 0.32). A notable multiplicative interaction was observed between low 5mdC (%) and elevated blood lead levels to increase OR of DD, with OR and 95% CI was 9.51 (4.18 - 21.64). The findings provide evidence of the combined effects of reduced 5mdC (%) and high blood lead concentrations, increasing the OR of DD.