Environmental Health最新文献

Background: Neuroblastic tumours (neuroblastoma and ganglioneuroblastoma) are the most common childhood solid tumours outside the central nervous system, with a median age of diagnosis of 2 years. Temporal clustering of neuroblastic tumours in northern England and Ontario, Canada has been previously reported.

Methods: We extracted data from the Scottish Cancer Registry to determine whether there was evidence of temporal clustering of neuroblastic tumours. Cases diagnosed in children and young adults aged 0-24 years between 2000 and 2020 were analysed. A modified version of the Potthoff-Whittinghill method was used to test for temporal clustering. Estimates of extra-Poisson variation (EPV) and standard errors (SE) were derived.

Results: One hundred and sixty-one cases of neuroblastic tumours, aged 0-24 years, were diagnosed during the study period. Overall, there was statistically significant temporal clustering between years within the full study period (EPV = 9.13, SE = 0.22, P < 0.001). In addition, for cases aged < 18 months, there was significant temporal clustering between months within quarters (EPV = 0.77, SE = 0.41, P = 0.044). For cases aged 18 months - 24 years, there was significant temporal clustering between fortnights within months (EPV = 1.00, SE = 0.47, P = 0.012).

Conclusions: The finding of temporal clustering is consistent with the involvement of one or more, as yet unknown, transient environmental agents in the aetiology of neuroblastic tumours.

Background: Policy-relevant spatial determinants of human exposure to Perfluoroalkyl Substances (PFAS), a broad class of persistent environmental contaminants affecting pregnancy and child development, remain poorly understood because of the diversity of exposure sources. This is especially true for modern, dense urban settings, which contain less well-studied built environment-related sources, including transportation-related ground and airborne contamination.

Methods: We link high-resolution spatiotemporal urban land use data to longitudinal residential histories to assess determinants of individual-level blood plasma PFAS exposures in two geographically- and demographically- diverse cohorts of pregnant women in urban Singapore (n = 784 in 2009-2011; n = 384 in 2015-2017). Longitudinal repeated measures allow us to rule out socio-behavioral factors (e.g., residential segregation) as alternative explanations. Actual land use occupancies were ground-truthed through automated extraction of Google Street View data.

Findings: Adjusting for known predictors and within-neighborhood unobserved spatial heterogeneity, a standard deviation (SD) increase (∼10,000m[Formula: see text]) in transport facility exposure was linked to 0.11 (1.78 ng/mL), 0.16, 0.11 SD increases in residents' perfluorobutane sulfonic acid (PFBS), perfluorobutanoic acid (PFBA), and perfluorononanoic acid (PFNA) concentrations, respectively, in the 2009 cohort. Dose-response analyses suggested that associations strengthened when transport facilities exceeded 10,000 m[Formula: see text], with residents living near ≥12,000 m[Formula: see text] exhibiting 7.3 ng/mL higher plasma PFBS (p = 0.04), consistent with footprints from large bus depots rather than smaller petrol kiosks. Associations with different PFAS congeners were replicated in the 2015 cohort. No other land use type showed similarly consistent findings.

Interpretations: Transport facilities are prevalent near residences in urban settings and may be potential sources of PFAS emissions from automotive-related lubricants, parts, and materials. Our findings that exposure was robustly associated with individual-level concentration, over and above behavioral and other factors, highlight the importance of monitoring these and other urban sources of exposure.

Background: Arsenic is a pervasive environmental contaminant and a recognized global public health concern. Experimental evidence suggests that arsenic may disrupt endocrine signaling during critical developmental windows, yet epidemiologic data on its effects on thyroid function in early childhood remain limited.

Methods: We investigated the cross-sectional association between arsenic exposure and free thyroxine (fT4) levels among 496 children aged 5 to 7 years enrolled in the Bangladesh Environmental Research in Children's Health (BiRCH) cohort. Arsenic exposure was assessed using urinary total arsenic and toenail arsenic concentrations. Serum fT4 levels were measured by an enzyme-linked immunosorbent assay (ELISA) kit. Associations with fT4 were estimated using multivariable linear regression models adjusted for child age, sex, body mass index, and environmental tobacco smoke exposure.

Results: The median urinary and toenail arsenic concentrations were 88.0 µg/L (interquartile range [IQR]: 127.4) and 1.7 µg/g (IQR: 2.0), respectively. Children in the highest quartile (Q4) of arsenic exposure had significantly higher fT4 levels compared to those in the lowest quartile (Q1), for both urinary (β = 0.09; 95% CI: 0.005-0.17) and toenail arsenic (β = 0.10; 95% CI: 0.03-0.17). A significant dose-response trend was observed across quartiles, suggesting a potential linear relationship.

Conclusions: Our findings suggest that thyroid function may be a sensitive target of arsenic toxicity in early childhood. Longitudinal studies are necessary to assess the long-term effects of early-life arsenic exposure on thyroid function across the life course.