International journal of hygiene and environmental health最新文献

Introduction

Perfluoroalkyl and polyfluoroalkyl substances (PFAS) are widely used in the manufacture of fluoropolymers. We evaluated biochemical and haematological effects of three PFAS, serum perfluorooctanoic acid (PFOA), ADV, and cC₆O₄ in workers of a fluoropolymer company.

Methods

Using data (2013–2022), we fitted random intercept regression models adjusted for several covariates and reciprocal adjustment between the three PFAS.

Results

We analysed data of 814 workers (698 men, 116 women), 607 from the chemical plant, 207 from the research centre, for a total of 4912 blood samples (2065 with all three PFAS measured). Median levels of PFOA and ADV were 21.3 and 120 μg/L. Most (65.5%) cC₆O₄ measurements were below the limits of quantification (which varied over time from 5 to 0.1 μg/L). For PFOA, we observed positive associations with total cholesterol (+1.1% increase per ln(PFOA) increase) and apolipoprotein B (+1.4%) and negative associations with alkaline phosphatase (−1.5%); suggestive associations were also found with RBC (−0.4%), IgA (−1.5%), IgM (−1.4%). ADV was positively associated with total and LDL cholesterol (+1.0% and +1.6% per ln(ADV) increase), apolipoprotein B (+1.0%), GGT (+2.1%), IgM (+1.4%), and WBC (+1.5%) and negatively associated with direct bilirubin (−2.3%) and alpha-2-globulins (−0.7%); suggestive associations were found for indirect bilirubin (−2.0%), oestradiol (−2.1%), ad CRP (+6.0%). For samples with detectable cC₆O₄ levels we observed higher values of ALP (+2.3%), proteins (+0.5%), IgG (+0.7%) and platelets (+1.6%) and suggestively increased total bilirubin (+3.9%), RBC (+0.6%), and oestradiol (+5.8%). Some associations (total cholesterol, apolipoprotein B, WBC, total bilirubin, and alkaline phosphatase showed reverse time trends in parallel with the strong decrease of serum PFOA and ADV over the study period.

Discussion

We found associations of serum PFOA and ADV with lipid metabolism, liver function, and immunoglobulins. The reverse time trends of some endpoints in parallel with decrease of serum PFOA and ADV reinforce causal interpretation of results. cC₆O₄ showed a different pattern of associations.

Background

Short-term exposure to low and high air temperatures can cause serious harmful effects on human health. Existing literature has mostly focused on associations of ambient air temperature with mortality and the need for health care in population-level studies. Studies that have considered self-perceived health status as an outcome when examining the effects of air temperature on health are scarce. In this study, we explored the short-term association of daily mean air temperature with various measures of self-perceived health status.

Methods

This cross-sectional analysis is based on the Cooperative Health Research in the Region of Augsburg (KORA) FIT study conducted in 2018/2019 and included participants from the Augsburg region of Southern Germany. Health-related quality of life (HRQOL) was evaluated by using the 5-level EuroQol Five Dimension (EQ-5D-5L) questionnaire, including the EuroQol visual analog scale (EQ-VAS). Self-rated health (SRH) and comparative self-rated health (CSRH) were each assessed using a single question. Daily mean air temperature data was estimated using a spatiotemporal model and assigned to participants' home addresses at a resolution of 1 × 1 km. Regression models with a Distributed Lag Non-linear Modeling (DLNM) approach were used to investigate the associations between daily mean air temperature and self-perceived health measures.

Results

We found no association of heat or cold with the HRQOL, SRH or CSRH. Nevertheless, there was a significant protective association of low air temperature with the EQ-5D-5L dimension “usual activities.”

Conclusion

There was no evidence of daily mean air temperature adversely affecting participants' self-perceived health status.

Background

Heat-related mortality has become a growing public health concern in light of climate change. However, few studies have quantified the climate-attributable health burden in Cyprus, a recognized climate change hotspot. This study aims to estimate the heat-related mortality in Cyprus for all future decades in the 21st century under moderate (SSP2-4.5) and extreme (SSP5-8.5) climate scenarios.

Methods

We applied distributed lag non-linear models to estimate the baseline associations between temperature and mortality from 2004 to 2019 (data obtained from Department of Meteorology of the Ministry of Agriculture, Rural Development and Environment and the Health Monitoring Unit of the Cyprus Ministry of Health). The relationships were then extrapolated to future daily mean temperatures derived from downscaled global climate projections from General Circulation Models. Attributable number of deaths were calculated to determine the excess heat-related health burden compared to the baseline decade of 2000–2009 in the additive scale. The analysis process was repeated for all-cause, cardiovascular, and respiratory mortality and mortality among males, females, and adults younger or older than 65. We assumed a static population and demographic structure, no adaptation to hot temperatures over time, and did not evaluate potential interaction between temperature and humidity.

Results

Compared to 2000–2009, heat-related total mortality is projected to increase by 2.7% (95% empirical confidence interval: 0.6, 4.0) and 4.75% (2.2, 7.1) by the end of the century in the moderate and extreme climate scenarios, respectively. Cardiovascular disease is expected to be an important cause of heat-related death with projected increases of 3.4% (0.7, 5.1) and 6% (2.6, 9.0) by the end of the century. Reducing carbon emission to the moderate scenario can help avoid 75% of the predicted increase in all-cause heat-related mortality by the end of the century relative to the extreme scenario.

Conclusions

Our findings suggest that climate change mitigation and sustainable adaptation strategies are crucial to reduce the anticipated heat-attributable health burden, particularly in Cyprus, where adaptation strategies such as air conditioning is nearing capacity.

Introduction

Lead poisoning contributes to a significant burden of disease as a toxic substance found in air, soil, and water. In Indonesia, the risk of exposure is high due to the inappropriate recycling of used lead batteries. The objective was to investigate the factors that influence lead levels in children's blood.

Methods

This cross-sectional study assessed blood lead levels (BLLs) in children aged 12–59 months in four communities exposed to used lead-acid batteries (ULABs) recycling activities, comparing them to a control area. The study employed a threshold level of 20 μg/dL to identify high BLLs and utilized a sample size of 324 children from exposed sites and 240 from control sites. Questionnaires, blood lead tests and a home-based assessment for environmental exposures were applied.

Results

The study participants comprised 295 boys and 269 girls, with an average age of 35 months. Significant disparities in soil lead concentrations median: Q1-Q3 were found between exposed (6581.7 : 2432.6–16647.1) ppm and control areas (253.5 : 158.8–417.1) ppm. Children in exposed areas had 3.9 times higher odds of BLL ≥20 μg/dL. Fathers with BLL ≥20 μg/dL had children with similarly elevated BLLs. Multivariate analysis identified socioeconomic status, study areas, environmental factors (cookware, food ware, spices, house cleaning), and children's behavior (breastfeeding duration) as determinants of elevated BLLs. Reported environmental factors had notable impact on BLLs, with aluminum cookware (aOR = 1.4, 95%CI [1.2–1.6]), food ware materials (aOR = 1.15, 95%CI [1.0–1.3]), type of spices (aOR = 2.7, 95%CI [1.7–48.0]), and house cleaning method (aOR = 2.9, 95%CI [1.2–7.1]).

Conclusion

This study highlighted key risk factors affecting children's blood lead levels (BLL) and emphasized the urgency of employing effective strategies to remediate lead-contaminated soils in exposed regions. The findings underscore the need for prompt medical intervention and monitoring for children in these areas, with additional research essential to fully understand lead poisoning pathways in the environment.

Purpose

Household air pollution is one of the leading causes of death and disease globally. Emerging evidence of elevated risk of neonatal death has been reported in Africa and South Asia. However, evidence on the extent of the problem in Latin America is limited despite the persistent use of highly polluting cooking fuels. We assessed whether the use of high-polluting household cooking fuels increases the risk of neonatal death compared to low-polluting fuels in Colombia.

Methods

We used cross-sectional data from the 2005–2015 Colombian Demographic Health Survey and performed a survey-featured multivariate logistic regression. We selected adjustment covariates based on a causal diagram, addressed missing data through multiple imputation, and conducted several sensitivity analysis, such as propensity score matching.

Result

We found evidence suggesting an increased risk of neonatal death in households using high-polluting fuels (OR: 1.48; 95% CI: 0.91, 2.39). The sensitivity analyses were consistent with the main analysis.

Conclusion

We observed increased odds of neonatal death associated with using high-polluting household cooking fuels compared to low-polluting fuels, although this association was not statistically significant. This study contributes evidence to a region where the issue is not yet a priority and should be included in national-level discussions and interventions that impact cooking fuel use patterns.

Background

On September 1976, due to the explosion of an ammonia-washing column at the petrochemical plant in Manfredonia (Italy), 39 tonnes of arsenic were released into the atmosphere, contaminating the plants and the neighbourhoods close to it. The aim of this study is to present the results of a 45-year follow up of exposed workers with a focus on residential exposure.

Methods

We contacted Italian General Registries Offices and updated the vital status of persons involved in the clean-up activities following the disaster. The outcome of interest was the overall and cause-specific mortality. An accelerated failure time (AFT) approach was used when appropriate to model the risk of mortality.

Results

1772 workers contributing 67,743 person years were considered in the analysis. For overall mortality, results of the age-adjusted AFT model show an accelerator factor of 0.89 (95%CI 0.80–0.99) among contract workers, which means a shortening of survival in comparison to the reference category (plastic area workers). When accounting for latency greater than 20 years, higher mortality rates for lung cancer were observed among workers residing in Manfredonia.

Discussion

An increased risk of mortality among workers who were more exposed to arsenic during the clean-up activities has been observed. In fact, a loss of 5 years of life among more exposed workers was calculated. Furthermore, the mortality rates of residents in Manfredonia were higher than those of workers residing elsewhere.

Antimicrobial resistance (AMR) is a global problem that gives serious cause for concern. Hospital wastewater (HWW) is an important link between the clinical setting and the natural environment, and an escape route for pathogens that cause hospital infections, including urinary tract infections (UTI). Bacteria of the genera Escherichia and Klebsiella are common etiological factors of UTI, especially in children, and they can cause short-term infections, as well as chronic conditions. ESBL-producing Escherichia and Klebsiella have also emerged as potential indicators for estimating the burden of antimicrobial resistance under environmental conditions and the spread of AMR between clinical settings and the natural environment. In this study, whole-genome sequencing and the nanopore technology were used to analyze the complete genomes of ESBL-producing E. coli and Klebsiella spp. and the HWW metagenome, and to characterize the mechanisms of AMR. The similarities and differences in the encoded mechanisms of AMR in clinical isolates (causing UTI) and environmental strains (isolated from HWW and the HWW metagenome) were analyzed. Special attention was paid to the genetic context and the mobility of antibiotic resistance genes (ARGs) to determine the common sources and potential transmission of these genes. The results of this study suggest that the spread of drug resistance from healthcare facilities via HWW is not limited to the direct transmission of resistant clonal lines that are typically found in the clinical setting, but it also involves the indirect transfer of mobile elements carrying ARGs between bacteria colonizing various environments. Hospital wastewater could offer a supportive environment for plasmid evolution through the insertion of new ARGs, including typical chromosomal regions. These results indicate that interlined environments (hospital patients – HWW) should be closely monitored to evaluate the potential transmission routes of drug resistance in bacteria.

Aim

To explore the effect of mixed exposure to per- and polyfluoroalkyl substances (PFAS) on metabolic syndrome (MetS).

Methods

This cross-sectional study used data from the Korean National Environmental Health Survey Cycle 4 (2018–2020). The serum concentrations of five PFAS (perfluorooctanoic acid [PFOA], perfluorooctanesulfonic acid [PFOS], perfluorohexanesulfonic acid, perfluorononanoic acid [PFNA], and perfluorodecanoic acid [PFDeA]) were measured, and the relative potency factor approach was employed for the mixture of PFAS (Cmix) assessment. MetS was diagnosed if the patient satisfied three of five criteria: central obesity, elevated triglycerides, reduced high-density lipoprotein cholesterol, elevated blood pressure (BP), and elevated glycated hemoglobin (HbA1c). Age, sex, smoking, drinking, and exercise status were considered as covariates. The risk of MetS for single and mixed exposure to PFAS was analyzed using binomial regression and Bayesian kernel machine regression (BKMR).

Results

A total of 2984 (male:female = 1:1.3; age range, 19–80 years) adults were enrolled. The prevalence of MetS was 45.6%. Each PFAS and Cmix levels were higher in participants with MetS than in those without MetS. Cmix increased the risk of elevated BP and HbA1c, and eventually MetS (odds ratio [OR] = 2.00, 95% confidence interval [CI] 1.11–3.60 per log₁₀Cmix; OR = 1.57, 95% CI 1.07–2.31 in the highest quartile of Cmix [Q4] vs. the lowest [Q1]). Sex-specific analyses revealed that the impact of Cmix was valid in females but not in males (Cmix Q4 vs. Q1: OR = 1.01, 95% CI 0.57–1.8 in males; OR = 2.30, 95% CI 1.38–3.84 in females). In the BKMR analysis, mixed exposure to PFAS dose-dependently increased the risk of MetS, particularly in females. Among single exposures, PFNA contributed significantly to the cumulative effect.

Conclusion

Mixed exposure to PFAS was associated with a higher risk of MetS in females. Further studies on potential health concerns associated with PFAS mixtures are warranted.

Exposure to environmental contaminants and the development of hypertension and diabetes represent crucial risk factors for chronic kidney disease (CKD). Toxicological studies have revealed that organophosphate esters (OPEs) impair kidney function. However, the joint effects of OPE exposure on kidney injury and the interactions of OPE exposure with hypertension or diabetes on kidney injury remain unclear. Our study aimed to investigate the individual and joint effects of OPE exposure on renal injury, as well as the potential interaction between OPE exposure and hypertension or diabetes on kidney injury. The study enrolled 1938 participants from Wuhan, China. To explore the relationship between OPE exposure and renal injury, we conducted multivariate linear and logistic regression analysis. The results indicated that each unit increase in 4-hydroxyphenyl diphenyl phosphate (4-HO-DPHP), bis(2-butoxyethyl) phosphate (BBOEP), and tris(2-chloroethyl) phosphate (TCEP) (1 μg/L-ln transformed) was associated with a decreased 0.57 mL/min/1.73 m² (95%CI: -1.05, −0.09), 0.85 mL/min/1.73 m² (95%CI: -1.52, −0.19) and 1.24 mL/min/1.73 m² (95%CI: -2.26, −0.23) of estimated glomerular filtration rate (eGFR), while each unit increase in 4-HO-DPHP and BBOEP (1 μg/L-ln transformed) was associated with 14% and 20% elevation of incident impaired renal function (IRF) risk. Notably the highest tertile of BCIPHIPP was positively associated with eGFR, although the p for trend ＞ 0.05. We employed Bayesian kernel machine regression (BKMR) and quartile-based g-computation (qgcomp) models to explore the joint effects of OPE mixtures on eGFR and IRF. Both the results of BKMR and qgcomp model consistently demonstrated negative associations between OPE mixtures and eGFR, and TCEP and 4-HO-DPHP were major contributors. Furthermore, we observed multiplicative interactions of diphenyl phosphate (DPHP), BBOEP, di-ocresyl phosphate (DoCP) & di-p-cresyl phosphate (DpCP), 1-hydroxy-2-propyl bis(1-chloro-2-propyl) phosphate (BCIPHIPP) and hypertension or diabetes on kidney injury (all P＜0.05). Those with diabetes or hypertension and higher OPE metabolite concentrations had increased risk of kidney function impairment compared to those who did not have diabetes or hypertension. These findings suggest that specific OPE exposure may elevate the risk of renal injury, particularly among hypertensive and diabetic populations.