Environmental Epidemiology最新文献

Background: Sex steroid hormones are critical for maintaining pregnancy and optimal fetal development. Air pollutants are potential endocrine disruptors that may disturb sex steroidogenesis during pregnancy, potentially leading to adverse health outcomes.

Methods: In the Environmental influences on Child Health Outcomes Understanding Pregnancy Signals and Infant Development pregnancy cohort (Rochester, NY), sex steroid concentrations were collected at study visits in early-, mid-, and late-pregnancy in 299 participants. Since these visits varied by the gestational age at blood draw, values were imputed at 14, 22, and 30 weeks gestation. Daily NO₂ and PM_2.5 concentrations were estimated using random forest models, with daily concentrations from each 1-km² grid containing the subject's residence. Associations between gestational week mean NO₂ and PM_2.5 concentrations and sex steroid concentrations were examined utilizing distributed lag nonlinear models.

Results: Each interquartile range (IQR = 9 ppb) increase in NO₂ during weeks 0-5 was associated with higher early-pregnancy total testosterone levels (cumulative β = 0.45 ln[ng/dl]; 95% CI = 0.07, 0.83), while each IQR increase in NO₂ during weeks 12-14 was associated with lower early-pregnancy total testosterone levels (cumulative β = -0.27 ln[ng/dl]; 95% CI = -0.53, -0.01). Similar NO₂ increases during gestational weeks 0-14 were associated with higher late-pregnancy estradiol concentrations (cumulative β = 0.29 ln[pg/ml]; 95% CI = 0.10, 0.49), while each IQR increase in NO₂ concentrations during gestational weeks 22-30 was associated with lower late-pregnancy estradiol concentrations (cumulative β = -0.18 ln[pg/ml]; 95% CI = -0.34, -0.02). No associations with PM_2.5 were observed, except for an IQR increase in PM_2.5 concentrations (IQR = 4 µg/m³) during gestational weeks 5-11 which was associated with lower late-pregnancy estriol levels (cumulative β = -0.16 ln[ng/ml]; 95% CI = -0.31, -0.00).

Conclusions: Residential NO₂ exposure was associated with altered sex steroid hormone concentrations during pregnancy with some indication of potential compensatory mechanisms.

Background: Few studies have investigated associations between per- and polyfluoroalkyl substances (PFAS) and childhood cancers. Detectable levels of PFAS in California water districts were reported in the Third Unregulated Contaminant Monitoring Rule for 2013-2015.

Methods: Geocoded residences at birth were linked to corresponding water district boundaries for 10,220 California-born children (aged 0-15 years) diagnosed with cancers (2000-2015) and 29,974 healthy controls. A pharmacokinetic model was used to predict average steady-state maternal serum concentrations of perfluorooctanesulfonic acid (PFOS) and perfluorooctanoic acid (PFOA) from contaminated drinking water. Adjusted odds ratios (AORs) and 95% confidence intervals (CIs) per doubling of background exposure were calculated for cancers with at least 90 cases.

Results: Predicted PFOS and PFOA maternal serum concentrations ranged from background (5 ng/ml PFOS and 2 ng/ml PFOA) to 22.89 ng/ml and 6.66 ng/ml, respectively. There were suggestive associations between PFOS and nonastrocytoma gliomas (n = 268; AOR = 1.26; 95% CI: 0.99, 1.60), acute myeloid leukemia (n = 500; AOR = 1.14; 95% CI: 0.94, 1.39), Wilms tumors (n = 556, AOR = 1.15; 95% CI: 0.96, 1.38), and noncentral system embryonal tumors (n = 2,880; AOR = 1.07; 95% CI: 0.98, 1.17), and between PFOA and non-Hodgkin lymphoma (n = 384; AOR = 1.19; 95% CI: 0.95, 1.49). Among children of Mexico-born mothers, there was increased risk of Wilms tumor (n = 101; AOR_PFOS = 1.52; 95% CI: 1.06, 2.18; AOR_PFOA = 1.59, 95% CI: 1.12, 2.24) and noncentral system embryonal tumors (n = 557; AOR_PFOS = 1.24, 95% CI: 1.03, 1.50; AOR_PFOA = 1.19, 95% CI: 0.98, 1.45).

Conclusion: Results suggest associations between predicted prenatal maternal PFAS serum concentrations and some childhood cancers. Future analyses are warranted.

Background: Utility services for electricity, gas, heat, and hot water are necessities for everyday activities (e.g., lighting, cooking, and thermal safety). Utility outages can threaten health; however, information is limited on the prevalence of electricity, gas, heat, and hot water outages in representative studies. We characterized infrastructure-related electricity, gas, heat, and hot water outages in New York City (NYC) and within subgroups.

Methods: Using a representative 2022 survey of NYC adults (18+), we assessed the prevalence for 6+ hour utility outages and compared across building, demographic, and health subgroups. Building characteristics included age, number of floors, rental type, and owner/rental status. Demographics included household poverty, neighborhood poverty, and race/ethnicity. For health, we focused on cognitive impairment, electricity-dependent medical equipment use, and mental health conditions.

Results: Outages impacted 20% of NYC residents. Heat outages were nearly 3× and 2× more common in mid-rise and high-rise buildings respectively, vs. low-rise buildings. Similarly, hot water outages were 5× and over 6× more prevalent in mid-rise and high-rise residences. Renters faced 2× more heat and hot water outages compared with owners. Compared with low-poverty households, high-poverty households faced 2× more hot water outages. Residents with mental health conditions experienced more electricity (11% vs. 5%), heat (15% vs. 7%), and hot water (16% vs. 8%) outages compared with those without.

Conclusions: NYC utility outage prevalence varied by type with heat and hot water being most common. Disparities across building, sociodemographic, and health characteristics were also larger and more frequent for heat and hot water outages.

Background: Toxicological studies suggest neonicotinoids increase oxidative stress and inflammation, but few epidemiological studies have explored these effects.

Methods: National Health and Nutrition Examination Survey (NHANES) 2015-2016 data were used to estimate associations between neonicotinoid exposure and inflammatory markers, including the C-reactive protein-to-lymphocyte count ratio (CLR), monocyte-to-high-density lipoprotein ratio (MHR), monocyte-to-lymphocyte ratio (MLR), neutrophil-to-lymphocyte ratio (NLR), derived NLR (dNLR), lymphocyte-to-monocyte ratio, platelet-to-lymphocyte ratio (PLR), and systemic immune-inflammation index (SII) using linear and multinomial logistic regression models. Sex was evaluated as a potential modifier.

Results: Detection of any parent neonicotinoid (β = -0.62, 95% confidence interval [CI] = -0.98, -0.26) and imidacloprid (β = -0.48, 95% CI = -0.87, -0.10) was associated with decreased CLR. Clothianidin was linked to reduced MLR (β = -0.04, 95% CI = -0.07, -0.02), but increased lymphocyte-to-monocyte ratio (β = 0.52, 95% CI = 0.27, 0.77). Higher dNLR (β = 0.85; 95% CI = 0.26, 1.43) was noted with detection of any neonicotinoid metabolite. Moderately high PLR was observed with detection of any neonicotinoid metabolite (relative risk ratio [RRR] = 1.63, 95% CI = 1.27, 2.09) or 5-hydroxy-imidacloprid (RRR = 2.19, 95% CI = 1.40, 3.41). Sex-modified analyses showed positive associations in males and inverse associations in females for MHR (P _int = 0.099, clothianidin), PLR (P _int = 0.026, clothianidin), and SII (P _int = 0.056, any parent neonicotinoid; P _int = 0.002, clothianidin), while the opposite pattern was noted with CLR (P _int = 0.073, any parent neonicotinoid) and NLR (P _int = 0.084, clothianidin).

Conclusion: Neonicotinoids may be associated with inflammatory changes, with potential sexual dimorphism. Further studies are required to explore these findings.

Background: There is considerable heterogeneity in fine particulate matter (PM_2.5)-mortality associations between studies, potentially due to differences in exposure assessment methods. Our aim was to evaluate associations of PM_2.5 predicted from different models with nonaccidental and cause-specific mortality.

Methods: We followed 107,906 participants of the Nurses' Health Study cohort from 2001 to 2016. PM_2.5 concentrations were estimated from spatiotemporal models developed by researchers at the University of Washington (UW), Pennsylvania State University (PSU), and Harvard TH Chan School of Public Health (HSPH). We calculated 12-month moving average concentrations and we used time-varying Cox proportional hazard ratios (HRs).

Results: There were 30,242 nonaccidental deaths in 1,435,098 person-years. We observed high correlations and similar temporal trends between the PM_2.5 predictions. We found no associations of UW, PSU, or HSPH PM_2.5 with nonaccidental mortality, but suggestive positive associations with cancer, cardiovascular, and respiratory disease mortality. There were small differences in HRs between the PM_2.5 predictions. All three predictions showed the strongest associations with cancer mortality: HRs (95% confidence interval, expressed per 5 µg/m³ increase) were 1.06 (1.01, 1.12) for UW, 1.08 (1.03, 1.13) for PSU, and 1.05 (1.00, 1.10) for HSPH. In a subset restricted to participants who were always exposed to PM_2.5 below 12 µg/m³, we observed positive associations with nonaccidental mortality.

Conclusion: We found that differences between PM_2.5 exposure assessment methods could lead to minor differences in strengths of associations between PM_2.5 and cause-specific mortality in a population of US female nurses.

Background: Ambient fine particulate matter (PM_2.5) is a risk factor for atherosclerosis disease. We aimed to assess whether nitric oxide stable metabolites (NOx) and l-arginine mediate the association between PM_2.5 and carotid intima media thickness (cIMT) increase.

Methods: We selected 251 participants from the control group of GEA (Genetics of Atheroslerosis Disease Mexican) study (2008-2013) in Mexico City. Mediation models were carried out using pathway analyses, a special case of structural equation models.

Results: The median concentration of PM_2.5 area under the curve (auc) was 25.2 µg/m³ (interquartile range: 24.2-26.4 µg/m³). Employing participants with observed values for both biomarkers (n = 117), the total effect of PM_2.5auc on mean cIMT at bilateral, right, and left was 19.27 µm (95% confidence interval [CI]: 5.77, 32.78; P value = 0.005), 12.69 µm (95% CI: 0.67, 24.71; P value = 0.039), and 25.86 µm (95% CI: 3.18, 48.53; P value = 0.025) per each 1 µg/m³ increase of PM_2.5auc. The direct effect of PM_2.5auc (per 1 µg/m³ increase) was 18.89 µm (95% CI: 5.37, 32.41; P value = 0.006) for bilateral, 13.65 µm (95% CI: 0.76, 26.55; P value = 0.038) for right, and 24.13 µm (95% CI: 3.22, 45.03; P value = 0.024) for left. The indirect effects of NOx and l-arginine were not statistically significant showing that endothelial function biomarkers did not mediate PM_2.5 and cIMT associations. Although l-arginine was not a mediator in the PM_2.5 and cIMT pathway, a decrease in l-arginine was significantly associated with PM_2.5auc.

Conclusions: In this study of adults from Mexico City, we found that PM_2.5 was associated with an increase in cIMT at bilateral, left, and right, and these associations were not mediated by endothelial function biomarkers (l-arginine and NOx).

Environmental epidemiologists are increasingly evaluating whether and how human exposure to vegetation (greenspace) can benefit health. Relatedly, scientists and policymakers have highlighted the need to integrate efforts to address the dual crises of accelerating climate change and rapid loss of biodiversity, including nature-based solutions. Greenspace is one solution that can protect humans from climate-related exposures, including heat, air pollution, and flooding. However, most environmental epidemiology research on greenspace occurs in high-income countries, and adverse birth outcomes, previously associated with greenspace, disproportionately occur in low- and middle-income countries (LMICs). Although epidemiology research using existing survey or administrative data and satellite imagery is important for documenting broad patterns, such research is lacking in LMICs. Further, complementary, community-engaged research to inform interventions and policies is needed so that nature-based solutions with co-benefits for climate mitigation and health are adopted effectively and equitably. We provide suggestions for future research that would increase impact and call for better representation of LMICs and vulnerable communities within high-income countries in research and action on greenspace and climate-sensitive birth outcomes.

Background: Per- and polyfluoroalkyl substances (PFAS) are a class of persistent synthetic chemicals that are found in human milk and are associated with negative health effects. Research suggests that PFAS affect both lactation and the human metabolome.

Methods: We measured perfluorooctanoate (PFOA) and perfluorooctane sulfonate (PFOS) in the milk of 425 participants from the New Hampshire Birth Cohort Study using liquid chromatography-tandem mass spectrometry (LC-MS/MS). A nontargeted metabolomics assay was performed using LC with high-resolution MS, and metabolites were identified based on in-house database matching. We observed six metabolic profiles among our milk samples using self-organizing maps, and multinomial logistic regression was used to identify sociodemographic and perinatal predictors of these profiles, including infant sex, parity, participant body mass index, participant age, education, race, smoking status, gestational weight gain, and infant age at time of milk collection.

Results: Elevated PFOA was associated with profiles containing higher amounts of triglyceride fatty acids, glycerophospholipids and sphingolipids, and carnitine metabolites, as well as lower amounts of lactose and creatine phosphate. Lower concentrations of milk PFOS were associated with lower levels of fatty acids.

Conclusion: Our findings suggest that elevated PFOA in human milk is related to metabolomic profiles consistent with enlarged milk fat globule membranes and altered fatty acid metabolism. Further, our study supports the theory that PFAS share mammary epithelial membrane transport mechanisms with fatty acids and associate with metabolic markers of reduced milk production.

Background: Sleep is influenced by the environments that we experience while awake and while asleep. Neighborhood walkability has been linked with chronic disease and lifestyle factors, such as physical activity; however, evidence for the association between walkability and sleep is mixed. Extant studies assign walkability based on residential addresses, which does not account for mobility. We examined the association between walkability and sleep in the Nurses' Health Study 3 (NHS3) Mobile Health Substudy (MHS).

Methods: From 2018 to 2020, individuals in the United States-based NHS3 prospective cohort participated in the MHS, in which minute-level global positioning systems (GPS) data and objective sleep duration and efficiency measures were collected via a custom smartphone application and Fitbit, respectively, for four 7-day periods across a year to capture seasonal variability. Census tract walkability was calculated by summing z-scores of population density (2015-2019 American Community Survey), business density (2018 Infogroup), and intersection density (2018 TIGER/Line road shapefiles). We ran generalized additive mixed models with penalized splines to estimate the association between walkability and sleep, adjusting for individual-level covariates as well as GPS-based exposure to environmental and contextual factors.

Results: The average main sleep period duration was 7.9 hours and the mean sleep efficiency was 93%. For both sleep duration and sleep efficiency, we did not observe an association with daily average walkability exposure.

Conclusion: In this study of women across the United States, we found that daily GPS-based neighborhood walkability exposure during wake time was not associated with objective wearable-derived sleep duration or sleep efficiency.