Environmental Health最新文献

Background: Acetaminophen is the most commonly used over-the-counter pain and fever medication taken during pregnancy, with > 50% of pregnant women using acetaminophen worldwide. Numerous well-designed studies have indicated that pregnant mothers exposed to acetaminophen have children diagnosed with neurodevelopmental disorders (NDDs), including autism spectrum disorder (ASD) and attention-deficit/hyperactivity disorder (ADHD), at higher rates than children of pregnant mothers who were not exposed to acetaminophen.

Methods: We applied the Navigation Guide methodology to the scientific literature to comprehensively and objectively examine the association between prenatal acetaminophen exposure and NDDs and related symptomology in offspring. We conducted a systematic PubMed search through February 25, 2025, using predefined inclusion criteria and rated studies based on risk of bias and strength of evidence. Due to substantial heterogeneity, we opted for a qualitative synthesis, consistent with the Navigation Guide's focus on environmental health evidence.

Results: We identified 46 studies for inclusion in our analysis. Of these, 27 studies reported positive associations (significant links to NDDs), 9 showed null associations (no significant link), and 4 indicated negative associations (protective effects). Higher-quality studies were more likely to show positive associations. Overall, the majority of the studies reported positive associations of prenatal acetaminophen use with ADHD, ASD, or NDDs in offspring, with risk-of-bias and strength-of-evidence ratings informing the overall synthesis.

Conclusions: Our analyses using the Navigation Guide thus support evidence consistent with an association between acetaminophen exposure during pregnancy and increased incidence of NDDs. Appropriate and immediate steps should be taken to advise pregnant women to limit acetaminophen consumption to protect their offspring's neurodevelopment.

Background: Fine particulate matter (PM_2.5) is associated with cardiovascular morbidity, especially among individuals with pre-existing cardiovascular conditions, such as heart failure (HF). Medical management with β-blockers may modify the association between PM_2.5 and heart rate (HR) as β-blockers act on similar neurophysiologic pathways as PM_2.5.

Methods: To examine potential medication-PM_2.5 interactions, we utilized electronic health records (EHRs) from 26,653 individuals with HF in North Carolina observed from 2014 to 2016. Linear mixed effect models with a random intercept for individual were adjusted for individual and census level demographics and socioeconomic confounders. We examined 0-4-daily PM_2.5 lags as well as the 5-day moving average. We stratified observations based β-blocker prescription status and quantified differences using a multiplicative interaction model. We also utilized data from an in vivo study of diesel exhaust exposure and β-blocker usage in HF prone rats to validate results and examine additional outcomes unavailable in the EHR data.

Results: Stratified analyses and the multiplicative interaction model revealed a significant difference in the association between PM_2.5 and HR based on β-blocker prescription status. For 5-day average PM_2.5 we observed a significant interaction (β_interaction = -0.68, 95% CI: -0.82, -0.55) indicating that the association between PM_2.5 and HR decreased for observations occurring after prescription of a β-blocker to study participants. This observation was reflected in the in vivo study as well.

Conclusions: β-blocker usage likely attenuates associations between short-term PM_2.5 and HR. Accounting for this in future studies may reveal novel means of reducing PM_2.5-related cardiovascular morbidity and reduce confounding in population with high rates of β-blocker usage.

Background: Ambient air pollution exposure during and before the pregnancy could result in adverse birth outcomes. This study uses data from women undergoing in vitro fertilization (IVF) data to investigate the associations between ambient air pollution exposure and adverse birth outcomes.

Methods: This study analyses the associations between adverse birth outcomes, namely low birth weight (LBW), small for gestational age (SGA), and preterm birth and daily mean air pollution exposure during each of four IVF windows. The air pollutants considered were particulate matter with an aerodynamic diameter of less than 10 µm (PM₁₀) and 2.5 µm (PM_2.5), as well as nitrogen dioxide (NO₂), which were estimated using the Atmospheric Dispersion Modelling System (ADMS-Urban). This data was linked to the IVF patients' postcode providing estimates of exposure to air pollutants. Logistic regression models were used to quantify the associations between air pollution exposure and adverse birth outcomes, and conditioning confounding factors. A subgroup analysis was conducted to investigate the differences in the effects of ambient air pollution exposure on the ICSI and IVF groups.

Results: From January 2010 to May 2018, there are 2069 babies were able to be included in this study. We found no significant associations between air pollution exposure and the risk of adverse birth outcomes during window 1(85 days before oocyte retrieval) and 2 (14 days after gonadotrophin medication). With 1 µg⋅m^-3 increase in PM₁₀ concentration during window 3 (14 days after embryo transfer) and 4 (embryo transfer to delivery) led to a 5% (95% CI: 1.05-1.06) and 10% (95% CI: 1.01-1.21) increase in the odds of preterm birth, but not other outcomes. In window 3, every 1 µg⋅m^-3 increase in NO₂ concentrations resulted in a 2% (95% CI: 1.00 - 1.04) increase in the odds of LBW and a 3% (95% CI: 1.00 -1.05) increase in the odds of SGA but showed no effect for preterm birth. The results of the subgroup analysis suggest that the air pollution exposure may have a greater impact on the IVF group compared to the ICSI group.

Conclusion: The results suggest that exposure to air pollution during the very early stage of pregnancy (14 days after conception) may represent the most critical window of susceptibility to an increased risk of adverse birth outcomes.

Background and objective: To provide guidance on management strategies for chronic obstructive pulmonary disease (COPD), this study systematically analyzed the burden of the disease due to ozone (O₃) exposure in adults aged ≥ 65 years.

Methods: Data from the Global Burden of Disease Study 2021 were used to analyse trends in the age-standardized mortality rate (ASMR) for O₃-related COPD in the elderly (≥ 65 years). Age-period-cohort (APC) model was used to analyse independent age, period and cohort effects. Spearman's correlation coefficient assessed the relationship between ASMR and socio-demographic index (SDI). Decomposition analysis decomposed the drivers of change. Cross-country inequality analysis assessed health inequalities between countries. Frontier analysis estimated optimal health outcomes.

Results: From 1990 to 2021, the number of O₃-related COPD deaths in the elderly increased from 0.187 to 0.420 million globally. Male ASMR was higher than female ASMR and tended to decrease, whereas female adults ≥ 90 years of age had increased ASMR. ASMR is decreasing in 93 countries and increasing in 78 countries. The global burden of disease was largely driven by population and ageing, but low and low-middle SDI regions were positively affected by ageing, population and epidemiological changes. Global health inequalities remained pronounced, particularly in lower-developed countries. Frontier analyses also showed that countries and regions with lower levels of development had greater potential to improve the burden.

Conclusion: Despite an overall reduction in the disease burden, O₃-related COPD mortality remains a major health threat to the elderly, particularly in less developed countries and regions.

Introduction: Epidemiological studies have documented the health effects of long-term exposure to fine particulate matter, while there is a growing number of studies looking into associations with one of its main components elemental carbon (EC) and its related metrics such as black carbon (BC), black smoke (BS) or aerosol light absorption coefficient often referred as "PM absorbance". We performed a systematic review and meta-analysis on the associations between long-term exposure to elemental carbon (EC) and disease incidence.

Methods: We searched for studies published up to April 2025, assessing long-term to EC-related exposure (also including BC, BS, PM absorbance) and incidence of ischemic heart disease (IHD), asthma, chronic obstructive pulmonary disease (COPD) and lung cancer in adults, and asthma and acute lower respiratory infections (ALRI) in children. We pooled effect estimates by random-effects models and investigated heterogeneity by region and risk of bias assessments. The certainty of the evidence was assessed using the Grading of Recommendations Assessment Development approach.

Results: We included 51 studies assessing long-term exposure to EC and disease incidence. The pooled relative risk (RR) for a 1 µg/m³ increase in EC was 1.10 (95% confidence interval (CI): 1.04, 1.17), 1.11 (95% CI: 1.00, 1.05), for incidence of lung cancer and IHD in adults, while a null association was observed for COPD risk. We estimated RR 1.06 (95% CI: 0.94, 1.21) and 1.37 (95% CI: 0.89, 2.04) for asthma and ALRI in children respectively. There was moderate to high heterogeneity in all associations, with the exception of lung cancer incidence for which the certainty of evidence was rated high.

Conclusions: Our meta-analysis supports an increased risk of lung cancer following long term exposure to EC and indicates associations for IHD in adults and respiratory outcomes in children. Although the evidence base on the effects of EC on diseases incidence has been increasing, further research is needed in the associations between long- term exposure to EC and various diseases' incidence.

Background: Some engine exhausts (EEs) have been classified as carcinogens and/or can have hormone-modulating properties that could play a role in prostate cancer development.

Objective: We investigated associations between lifetime occupational exposure to various EEs and prostate cancer risk, overall and for aggressive cancers.

Methods: In a population-based case-control study conducted in Montreal, Canada, 1,924 incident histologically-confirmed prostate cancer cases (436 aggressive) and 1,989 population controls were recruited. Socio-demographics, lifestyle factors and a detailed occupational history were collected during in-person interviews. Industrial hygienists conducted evaluations of intensity, frequency and reliability of exposure to EEs resulting from the combustion of several fuels (any diesel, light- and heavy-duty diesel, leaded and unleaded gasoline, propane and jet fuel) in each job held ≥ 2 years. Odds ratios (ORs) and 95% confidence intervals (CI) were estimated for exposure to each EE, in association with prostate cancer risk, adjusting for age and then for potential lifestyle and occupational confounders, accounting for a 5-year latency period. As most associations were not linear, we fitted functions for changes in percentile distributions based on natural cubic splines.

Results: There was no evidence of associations between exposure to the various EEs and overall prostate cancer. However, for high-grade cancers, based on the fully-adjusted model, a change from the 25th to the 75th percentile of the exposure distribution of any diesel EE yielded an OR of 1.24 (95%CI 0.96-1.61), and of 1.27 (95% CI 0.80-2.01) for a change from the 75th to the 95th percentile. These increases reflected exposure to diesel EE from light-duty vehicles, associated with similar ORs. For leaded gasoline EE, a change from the 75th to the 95th percentile resulted in an age-adjusted OR of 1.36 (95%CI 0.88-2.11), which was attenuated to 1.12 (95%CI 0.63-2.02) after full adjustment. There were no associations with EE from unleaded gasoline, diesel from heavy-duty vehicles, jet fuel and propane.

Conclusion: There was suggestive evidence for a deleterious role of occupational exposure to EE resulting from the combustion of any diesel, light-duty diesel and from leaded gasoline in the development of aggressive prostate cancer. Results were independent from prostate cancer screening patterns.

Background: Exposure to mold and solid cooking fuels represents a significant environmental health concern, contributing substantially to indoor air pollution among elderly populations. However, the association between mold exposure, household fuel use, and mental health remains poorly understood. Here we examine individual and joint associations of these exposures on depression, anxiety, and their co-occurrence in older adults.

Methods: We evaluated 9,243 elderly participants from the eighth survey wave of the Chinese Longitudinal Healthy Longevity Survey (CLHLS) to explore the associations between mold exposure, solid fuel use, and depression, anxiety, and their co-occurrence. Multivariable logistic regression models were employed to quantify these relationships, with adjusted odds ratios (aOR) and 95% confidence intervals (CI) reported.

Results: The study identified a depression prevalence of 13.61% and an anxiety prevalence of 11.79%. Participants exposed to mold demonstrated significantly higher odds of depression (OR = 2.26, 95% CI = 1.93-2.63), anxiety (OR = 2.11, 95% CI = 1.80-2.48), and their co-occurrence (OR = 2.58, 95% CI = 2.10-3.16), compared to participants without mold exposure. Moreover, the use of solid fuels for cooking, as opposed to clean fuels, was correlated with higher occurrence of depression (OR = 1.27, 95% CI = 1.10-1.47), anxiety (OR = 1.31, 95% CI = 1.12-1.52), and their co-occurrence (OR = 1.36, 95% CI = 1.10-1.67). Notably, solid fuel use appeared to attenuate the association between mold exposure and anxiety (Relative excess risk due to interaction [RERI] = -0.22, 95% CI = -0.44, -0.01).

Conclusions: The study found that exposure to mold and use of solid fuels may be associated with higher prevalence of depression, anxiety, and their co-occurrence. Further prospective studies are warranted to validate our findings.

Background: Air pollution is widely associated with allergic diseases, including asthma. Although previous studies have suggested an epidemiological link between air pollution and asthma, the combined effects of air pollutants and polygenic risk scores (PRSs) on asthma risk remain incompletely understood. This study aimed to examine the impact of air pollutants and PRS on asthma risk among patients in a Taiwan medical institution.

Methods: This retrospective matched case-control study utilized data from the Taiwan Precision Medicine Initiative (TPMI) project to compare asthma patients with a non-asthmatic control group. Participants were stratified into quartiles based on their asthma PRS, while air pollutant exposure was assessed by both duration and concentration. Conducted at Taichung Veterans General Hospital, the study followed participants from January 1, 2000, to December 31, 2021. Logistic regression was used to analyze the relationships between air pollution exposure, genetic risk, and asthma incidence.

Results: A total of 9,756 participants were included (3,252 asthma patients and 6,504 controls). Individuals in the highest PRS quartile demonstrated a significantly increased asthma risk (odds ratio = 1.532, 95% CI = 1.333-1.762, p < 0.0001). Long-term exposure to low levels of PM_2.5, PM₁₀, NO₂, Mn, and O₃ further elevated asthma risk, with the association becoming more pronounced under conditions of high air pollution.

Conclusion: Long-term exposure to low concentrations of air pollutants significantly increases asthma risk, especially among individuals with high genetic susceptibility. These findings emphasize the importance of personalized health management for individuals with elevated PRS.

Trial registration: Not applicable.

Background: Maternal prenatal exposures to per- and polyfluoroalkyl substances (PFAS) have been linked to adverse birth outcomes. However, few investigations have considered paternal PFAS exposure. We estimated the parent-specific associations of prenatal PFAS exposures with adverse birth outcomes.

Methods: This study included 498 couples from the INUENDO cohort recruited at antenatal care visits in Greenland, Poland, and Ukraine during 2002-2004. We measured five major types of PFAS in parental serum during pregnancy. We analyzed three birth outcomes ascertained from medical records, including gestational age, birth weight, and birth length. We used weighted least squares linear regression to evaluate parent-specific associations of serum PFAS with the birth outcomes, adjusting for parental co-exposures and covariates. We also used quantile g-computation for mixture modeling of the birth outcomes of paternal and/or maternal exposures to multiple PFAS.

Results: No associations were found between maternal and paternal PFAS exposures and gestational age. However, after adjusting for paternal PFOA, a higher level of maternal serum perfluorooctanoate (PFOA) was linked to a tendency towards lower birth weight and shorter birth length. Paternal exposure to several PFAS was also associated with a tendency for shorter birth length, but the estimated effect sizes were small. We found no joint exposure effects in the mixture analyses.

Conclusions: While the evidence was inconclusive, maternal PFOA and paternal PFAS exposures seemed to be associated with lower offspring birth weight and shorter birth length, respectively. Parent-specific effects of PFAS exposures on offspring growth and development warrant further research.

Pregnant women are regularly exposed to a variety of environmental toxicants in daily life, posing a potential threat of kidney injury before presence of clinical manifestations. As there is a paucity of studies employing an exposome-based approach of kidney health in pregnant women, this study utilizes the above-mentioned strategy to identify the most significant environmental toxicants associated with early kidney injury in pregnant women in the cohort of TMICS (Taiwan Maternal and Infant Cohort Study). A total of 1,139 third-trimester pregnant women (weeks 29-40) were recruited between 2012 and 2015, and one-spot urine samples were successfully collected for study. Sixteen biomonitoring chemicals were measured in urine, including exposure measurements of melamine, 9 phthalate metabolites, nonylphenol (NP), bisphenol A (BPA), methylparaben (MP), ethylparaben (EP), propylparaben (PP), and butylparaben (BP), and outcome measurements of NAG (N-acetyl-β-d-glucosaminidase) and albumin-to-creatinine ratio (ACR). A two-tier strategy of statistical analyses was employed and data was randomly and evenly split to both training (n = 569) and validation (n = 570) sets. Using a weighted quantile sum (WQS) regression in the training set and subsequently a multivariate regression in the validation set, we found that NP was the most important chemical to link with early markers of kidney injury, both ACR and NAG. Our findings indicate that short-term exposure to NP is associated with markers of subclinical kidney injury in pregnant women in Taiwan. Further research is warranted to determine whether NP exposure is linked to clinically relevant kidney outcomes.