Environmental Health最新文献

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.

Background: Polybrominated diphenyl ethers (PBDEs) and organophosphate esters (OPEs) are commonly used as flame retardants. Limited research exists on socioeconomic and racial/ethnic disparities in exposure to these compounds and their impact on executive functioning (EF) in early childhood. The present study examined independent and joint effects of income and race/ethnicity on flame retardant exposure in early childhood and investigated associations between flame retardant exposure and children's EF.

Methods: This cross-sectional study used data from 349 preschool children recruited in Oregon. Children wore silicone wristband samplers for seven days, with exposures to 41 flame retardant compounds analyzed by gas chromatography mass spectrometry. We focused on exposure to 6 compounds (BDE 47, BDE 99, BDE100, TCPP, TDCPP, TPP) and two composite indices (ΣPBDE, ΣOPE). Wilcoxon rank-sum tests examined exposure differences by race/ethnicity and income (low income = below federal poverty level). Multiple linear regression models, nested within classrooms, assessed the association between PBDE and OPE exposure and EF, measured by the Head-Toes-Knees-Shoulders-Revised (HTKS-R) and Dimensional Change Card Sort (DCCS) tasks.

Results: Children were 5.1 years old (SD = 0.3), 29.9% were from underserved racial/ethnic backgrounds, and 27.8% of families were low income. Compared with higher income families, children from low income families were exposed to 83.4% greater ΣPBDE exposures and 36% greater TDCPP exposures. There was no evidence of racial/ethnic disparities in PBDE or OPE exposures. Controlling for age, sex, income, race/ethnicity, and disability or cognitive delay, neither PBDE nor OPE exposures were consistently related to EF, but children from lower income families scored 28.6% lower on the HTKS-R, and children from underserved races/ethnicities scored 25.9% lower on the HTKS-R.

Conclusions: Our findings highlight persistent income disparities in PBDE exposures at a pivotal point in children's development, and reveal similar disparities in TDCPP exposures. Furthermore, socioeconomic disadvantage was more strongly associated with reduced EF than either PBDE or OPFR exposures. These findings underscore the need to address structural social inequities, and also highlight the need for greater representation of children from underserved backgrounds in research that seeks to characterize chemical and social exposures within neighborhood and preschool environments.

Introduction: Aflatoxins are environmental hazards; potent carcinogenic and immunosuppressive agents that contaminates corn and other crops. A high proportion of hepatocellular carcinoma cases are caused by exposure to dietary aflatoxins. Cervical cancer is common among Ugandan women; this malignancy is caused by persistent infection with oncogenic HPV types. An analysis was performed to examine associations between plasma aflatoxin B₁ (AFB₁) detection and oncogenic HPV detection (HPV types 16, 18, 31, 33, 35, 39, 45, 51, 52, 56, 58, 59, 66, and 68) and persistence among Ugandan women.

Methods: Ugandan women were enrolled in a prospective cohort study. Annual cervical swabs (Enrollment, Month 12 and Month 24) were tested for oncogenic HPV. Plasma AFB₁ concentration was measured (as AFB₁-lysine conjugate, or AFB₁-lys) at Enrollment and Month 12. Multivariable regression models were fitted to examine associations of plasma AFB₁-lys concentrations and oncogenic HPV controlling for demographic and behavioral characteristics.

Results: The analytical sample consisted of 114 women with a mean age of 33.2 years; 60 women were living with HIV; 59 were receiving antiretroviral therapy (ART) at enrollment. AFB₁-lysine adducts (AFB₁-lys) was detected in plasma from all 114 women. Multivariable regression models showed that plasma AFB₁-lys concentration was associated with a higher risk of detection of HPV 16 (OR = 2.64, 95% CI = 1.42-4.90, p = 0.002) and HPV 18 (OR = 2.24, 95% CI = 1.27-3.96, p = 0.005), and persistence of HPV 16 (OR = 3.16, 95% CI = 1.59-6.26, p = 0.001) and HPV 18 (OR = 2.06, 95% CI = 1.09-3.90, p = 0.025), controlling for age, marital status, years of education, home ownership, distance to health care, number of lifetime sex partners, age of first sex, and HIV status.

Conclusions: AFB₁ is an environmental hazard that is prevalent among Ugandan women. Higher plasma AFB₁-lys concentration was associated with detection and persistence of HPV 16 and HPV 18; this association was independent of HIV status. As a result, these women may be at increased risk of cervical cancer. Further studies are needed to determine the mechanisms involved.

Background: Exposure to high levels of vehicle traffic during childhood seems to have a negative effect on lung function. Less is known about the effects of exposure to relatively low levels during childhood. We aimed to study how exposure to vehicle traffic in childhood is associated with lung function and asthma in young adulthood in a 10-year follow-up of a population-based cohort in a municipality with relatively low levels of vehicle traffic.

Methods: The Obstructive Lung Disease in Northern Sweden (OLIN) pediatric cohort II was recruited in 2006 at age 8 years. Exposure to vehicle traffic at baseline was studied in relation to lung function at follow-up at age 19 years (n = 1056 participants). Lung function measures included FEV₁, FVC and FEV₁/FVC. Different exposure thresholds were defined based on proximity (within a 200 m radius from the home address) to a road with a minimum daily count of heavy vehicles (≥ 250 and ≥ 500) or any type of vehicle (≥ 4000 and ≥ 8000). The association between exposure to vehicle traffic at baseline and lung function at follow-up was analyzed by linear regression adjusting for potential confounders.

Results: In general, those above the exposure thresholds had lower lung function than those below, but not significantly so in all comparisons. Those exposed to ≥ 250 heavy vehicles/day had lower mean FEV₁ z-score at follow-up (-0.38) compared with those exposed to < 250 heavy vehicles/day (-0.21), p = 0.033, and this association remained after adjustment for confounders (p = 0.036). Also, those exposed to ≥ 8000 vehicles/day had lower mean FVC z-score (-0.19) than those exposed to < 8000 vehicles/day (-0.02), p = 0.047, with p = 0.032 after adjustment.

Conclusions: Exposure to vehicle traffic in childhood, in a relatively low traffic-flow environment, may be associated with a slightly lower lung function in young adulthood.