Environmental Epidemiology最新文献

Background: Folate plays a critical role during pregnancy, preventing neural tube defects and possibly adverse neurodevelopment. Per- and polyfluoroalkyl substances (PFAS) are synthetic chemicals that may decrease folate levels. Although some studies have found associations between PFAS and folate, we are unaware of studies conducted in pregnant women. To address this knowledge gap, we evaluated associations between PFAS and whole blood folate (WBF) in pregnant women.

Methods: We used data from 288 pregnant women in the Health Outcomes and Measures of the Environment (HOME) Study, a pregnancy and birth cohort in the Cincinnati Ohio area. We measured eight serum PFAS and WBF concentrations at 16 weeks' gestation. We used linear regression to estimate the effect of each PFAS on WBF, and quantile-based g-computation and Bayesian kernel machine regression (BKMR) to investigate the joint effect of PFAS on WBF, adjusting for parity, prenatal vitamin intake, maternal race/ethnicity, household income, maternal age, and second trimester smoking status in all models. In addition, we investigated interactions between PFAS using BKMR.

Results: We did not observe inverse associations of individual PFAS or their mixture with WBF, nor interactions between PFAS in the BKMR model in pregnant women.

Conclusion: Future studies could consider WBF measures in late pregnancy to evaluate other periods of susceptibility. Furthermore, as people are exposed to multiple PFAS, future studies should continue to consider joint PFAS exposure.

Background: Non-nutritive suck (NNS) is a measure of neurofunction sensitive to environmental exposures in utero. This study aimed to evaluate the relationship between gestational phenol exposure and NNS patterning.

Methods: Mother-infant pairs from two diverse prospective cohorts were enrolled in the Environmental influences on Child Health Outcomes Program. Phenols were measured in prenatal maternal urine samples and adjusted for specific gravity. NNS was sampled in 1-8-week-old infants using a custom pacifier for ~5 minutes. Associations of 11 phenols and triclocarban with 5 NNS outcomes were assessed individually and as a mixture using generalized linear models adjusted for cohort, child sex and assessment age, and maternal age and education.

Results: Altogether, 215 mother-infant pairs were included. Bisphenol-F was related to a lower NNS frequency. Triclosan was associated with a higher NNS frequency. Propylparaben, 2,4-dichlorophenol, and 2,5-dichlorophenol were associated with lower NNS amplitude. Benzophenone-3, 2,4-dichlorophenol, and 2,5-dichlorophenol were related to more NNS bursts/minute. Propylparaben was associated with more NNS cycles/bursts. Seven phenols were included in mixture analyses: 2,4-dichlorophenol, 2,5-dichlorophenol, benzophenone-3, bisphenol-A, bisphenol-S, methylparaben, and propylparaben. Both Bayesian kernel machine regression and quantile g-computation showed that higher concentrations of the mixture were associated with lower amplitude but more bursts/minute and cycles/burst. Propylparaben was important in the overall mixture effect on amplitude, whereas benzophenone-3 was important in the relationship with bursts/minute.

Conclusions: Gestational phenol exposure is linked to altered NNS patterning in neonates. Future work should further investigate phenol mixture effects, potential mechanisms, and the association of altered NNS with neurodevelopment.

Background: New national power outage exposure data have become available since 2020, which can support epidemiologic studies of power outage and health outcomes, but exposure assessment challenges remain. Two sources of bias could affect results: available datasets are missing large percentages of observations, and the health-relevant duration of power outages remains unknown. Here, we aimed to determine if existing datasets can produce usable effect estimates in epidemiologic studies despite missing data, and quantify bias introduced by incorrect assumptions about the health-relevant duration of power outages.

Methods: Based on existing data from PowerOutage.us, we conducted simulations representing a county-level study. We simulated and then estimated the effect of daily power outage exposure on hospitalization rates. We measured the magnitude and direction of bias introduced in the presence of incorrect assumptions about the health-relevant power outage duration and when increasing amounts of exposure data were missing.

Results: When the health-relevant power outage duration was underestimated, results were substantially biased towards the null (mean bias: -64.7%, SD: 34.9). Overestimation of the health-relevant power outage duration resulted in smaller bias (mean bias: -6.7%, SD: 30.6). When 80% or more of county-level person-time of power outage data were missing in 80% of study counties, results were severely biased towards the null (mean bias: -54.4%, SD: 39.8).

Conclusions: Our results show that while some bias is likely, sensitivity analyses and careful choices of health-relevant duration can help researchers leverage available power outage data to produce low bias effect estimates in epidemiologic studies of power outages and health outcomes.

Background: Prenatal exposure to environmental chemicals may be associated with autism or autistic-like behaviors. Previous studies suggest that these associations are stronger when folic acid (FA) supplementation is lower.

Methods: We used data from the Maternal-Infant Research on Environmental Chemicals study, a Canadian pregnancy and birth cohort (2008-2011). We considered five separate chemical mixtures (measured during the first trimester of pregnancy): metals, organochlorine pesticides, per- and polyfluoroalkyl substances (PFAS), polychlorinated biphenyls (PCBs), and persistent organic pollutants (POPs; including organochlorine pesticides, PFAS, PCBs, and one polybrominated diphenyl ether congener). Autistic-like behaviors were documented in 601 3-4-year-old children with the social responsiveness scale-2 (SRS-2), where higher T-scores denote more behaviors. We used quantile g-computation to estimate the mixture-SRS-2 associations and assessed whether gestational FA supplementation and plasma total folate concentrations modified these associations.

Results: The PFAS mixture was associated with decreased SRS-2 T-scores (Ψ = -0.5; 95% confidence interval [CI] = -1.1, 0.1). The metal-SRS-2 associations were stronger in the positive direction among participants with high (>1,000 μg/d) FA supplementation (Ψ = 2.4; 95% CI = 0.8, 3.9) versus those with adequate (400-1,000 μg/d) supplementation (Ψ = -0.2; 95% CI = -1.1, 0.7) (p-interaction = 0.003). Plasma total folate concentrations similarly modified these associations (p-interaction = 0.01). The associations between the PFAS, PCB, and POP mixtures and SRS-2 T-scores were stronger in the positive direction among participants with low (<400 μg/d) versus adequate FA supplementation. This was not observed when assessing modification by plasma total folate concentrations.

Conclusion: Our results suggest that the metal mixture is more strongly associated with autistic-like behaviors among participants with higher folate exposure, and the PFAS, PCB, and POP mixtures are more strongly associated with autistic-like behaviors among participants with low FA supplementation.

Background: Characterization of US sociodemographic disparities in air pollution respiratory effects has often been limited by lack of participant diversity, geography, exposure characterization, and small sample size.

Methods: We included 34 sites comprising 23,234 children (born 1981-2021) from the Environmental influences on Child Health Outcomes (ECHO) Program with data on asthma diagnosis until age 10 (182,008 person-years). Predicted annual exposure to fine particulate matter (1988-2021), nitrogen dioxide (2000-2016), and ground ozone (2000-2016) were assigned based on residential histories. For each pollutant, we fitted time-varying Cox models adjusted for time trend, site, and several area- and individual-level sociodemographic features that were separately considered as modifiers via an interaction with exposure.

Results: The hazard ratio of incident asthma by age 10 years was 1.19 (95% CI = 1.10, 1.28), 1.19 (95% CI = 1.05, 1.34), and 1.11 (95% CI = 1.01, 1.22) of an interquartile range increase in prior-year exposure to fine particulate matter (6.17 µg/m³), nitrogen dioxide (15.37 ppb), and ozone (6.87 ppb), respectively. For both fine particulate and nitrogen dioxide, children from areas with a higher proportion of Black residents or with a higher population density had greater pollution-associated risks of incident asthma. For ozone, asthma risks were enhanced in less dense areas.

Conclusions: US efforts to mitigate childhood asthma risk by reducing air pollution would benefit from addressing root structural causes of vulnerability and susceptibility, including spatial patterning in air pollution sources and exposures as well as social and economic disadvantage.

Background: Prolonged exposure to sunlight increases the risk of skin cancer. However, multiple sunlight-related health benefits have been identified. The overall effect of sun exposure on mortality remains inconclusive. This study investigated the association between daylight exposure and mortality (all-cause and cause-specific: cancer, cardiovascular disease (CVD), and noncancer non-CVD mortalities).

Methods: This study utilized the Adventist Health Study (AHS) 2 cohort of North America. Sun exposure was defined using time spent outdoors during daylight in warmer and cooler months. Mortality outcomes were identified through 2015. Multivariable Cox regression was used to examine the association between sun exposure and mortality.

Results: This study included 83,205 AHS-2 participants enrolled between 2002 and 2007. We observed nonlinear (reverse J-shaped) associations between time outdoors in warmer months and the risks of all-cause, CVD, and noncancer non-CVD mortalities. Compared with spending 30 min/day during daylight in warmer months, spending 2 hours/day was associated with a lower risk of all-cause (hazard ratio: 0.90; 95% confidence interval = 0.86, 0.93), CVD (0.89; 0.83, 0.95), and noncancer non-CVD mortalities (0.83; 0.78, 0.89), but was not significantly associated with cancer mortality risk (1.02; 0.93, 1.13) after adjusting for physical activity and important confounders. All associations were weaker with the time spent outdoors in cooler months.

Conclusions: Moderate time outdoors in daylight during warmer months could be associated with lower risks of all-cause, CVD, and noncancer non-CVD mortality; however, there was no clear evidence of an association with cancer mortality. Epidemiological studies need to investigate the balance between sun exposure's health benefits and risks.

Background: Population-level interventions that promote healthy aging through modifications to the built environment are likely to be more effective than individual-level interventions. Few studies have examined the influence of multiple built environment factors on measures of healthy aging.

Objectives: We leveraged detailed data from a population-based cohort study to examine how multiple aspects of the built environment were associated with grip strength, a well-accepted measure of age-related health status.

Methods: A cross-sectional analysis was conducted among 15,068 participants of the British Columbia Generations Project. Geospatial measures of air pollution (PM_2.5, SO₂, and NO₂), greenness, light-at-night, and walkability were linked to participant residential postal codes. Grip strength was measured using a digital hydraulic hand dynamometer. Logistic regression analyses were used to estimate the odds of having sex-specific clinically weak measures of grip strength in association with each built environment factor. The other built environment factors, demographics, and lifestyle factors were evaluated as confounders.

Results: Increased SO₂ and greenness were statistically significantly associated with increased and decreased odds of having clinically weak grip strength, respectively, after adjusting for demographic, lifestyle, and other built environment factors.

Conclusion: Our findings suggest that built environment factors are compelling targets for improving age-related health, though the mechanisms underlying associations with these factors, particularly greenness, remain uncertain.

Background: This systematic review aimed to estimate relative risks for incident ischemic heart disease (IHD), myocardial infarction (MI), and stroke in relation to long-term road traffic noise exposure and to evaluate exposure-response functions.

Methods: We systematically searched databases for longitudinal studies in humans on incident IHD, MI, and/or stroke, including quantitative estimates on individual exposure to residential road traffic noise based on validated models or measurements. Risk of bias was evaluated in each study based on predefined criteria. Pooled linear exposure-response functions were generated from random-effect models in meta-analyses of study-specific risk estimates. Restricted cubic spline models were used to capture potential nonlinear associations.

Results: Twenty eligible studies were identified based on more than 8.4 million individuals, mostly from Europe, including between 160,000 and 240,000 cases for each of the outcomes. Pooled relative risk estimates were 1.017 (95% confidence interval [CI]: 0.990, 1.044) for IHD, 1.029 (95% CI: 1.011, 1.048) for MI, and 1.025 (95% CI: 1.009, 1.041) for stroke per 10 dB L_den in road traffic noise exposure. Risk estimates appeared higher in combined analyses of studies with a low risk of exposure assessment bias. Restricted cubic spline analyses of these studies showed clear risk increases with exposure for all three cardiovascular outcomes.

Conclusions: The evidence indicates that long-term exposure to road traffic noise increases the incidence of IHD, including MI, and stroke. Given the abundant exposure, traffic noise is a cardiovascular risk factor of public health importance. High-quality assessment of noise exposure appears essential for the risk estimation.

Residential relocation can be leveraged as a natural experiment. This study examined the changes in environmental exposures due to residential relocation in two samples of within-city movers in Bradford (UK); 2089 residents (66% women, mean [SD] age, 47.80 [19.88] years) with preexisting common mental disorders-related prescriptions and 12,699 residents (60% women, mean [SD] age, 42.47 [17.40] years) without the same prescriptions at baseline (January-April 2021). Study data were extracted from National Health Service health records. The outcome was the presence of an active prescription for anxiolytics or antidepressants (yes/no) 1 year after relocation (January-April 2022). Change scores were calculated for several exposures, including the normalized difference vegetation index, distance decay to green spaces, coarse (PM₁₀) and fine particulate matter (PM_2.5), and nitrogen dioxide (NO₂) at pre- and postmove addresses. Logistic regression models were used for each change score exposure, adjusting for covariates selected using a direct acyclic graph validated against the data. Participants without prescriptions at baseline were likely to relocate to less green and less polluted areas compared with those with preexisting medication. A total of 15% of participants without prescriptions at baseline had an active prescription at follow-up. For these, increases in normalized difference vegetation index were associated with lower odds of having active prescriptions at follow-up [OR (odds ratio) = 0.93 (95% confidence interval [CI] = 0.88, 0.98), P = 0.007], whereas increases in PM_2.5 [OR = 1.1 (95% CI = 1.04, 1.16), P < 0.001] and PM₁₀ [OR = 1.12 (95% CI = 1.06-1.19), P < 0.001] concentrations were associated with higher odds. Changes in environmental exposures due to residential relocation showed an influence on mental health only for those participants without active prescriptions in the baseline.

Background: Evidence of the association between fine particulate matter (PM_2.5) exposure and child neuropsychological function is equivocal. We examined early life PM_2.5 exposure in relation to fine motor function, attention, and working memory in early childhood.

Methods: We used data from the Spanish INfancia y Medio Ambiente Project, 2003-2008. Exposure to PM_2.5 (μg/m³) was assessed using spatiotemporal land-use random forest models and assigned based on residential address histories. Around age six, children completed the finger tapping test, attentional network test (ANT), and n-back task to evaluate fine motor speed, attention, and working memory, respectively. A total of 1,310 children had data from at least one neuropsychological assessment. General linear models were applied to assess associations between average prenatal and postnatal PM_2.5 with each outcome. Distributed lag nonlinear models were used to explore refined periods of susceptibility to PM_2.5. We reported β estimates and 99% credible intervals (CrI) representing the change in each outcome per 5-μg/m³ increase in PM_2.5.

Results: Prenatal PM_2.5 exposure was associated with decreased mean hit reaction time (HRT) (β = -21.82; 99% CrI = -64.1, 20.4) and HRT-standard error (β = -9.7; 99% CrI = -30.3, 10.9) on the ANT but estimates were imprecise. Postnatal PM_2.5 was associated with reduced mean HRT on the n-back task (β = -39.4; 99% CrI = -115.1, 26.3). We observed sensitive periods of exposure in the postnatal period associated with both better and worse performance on the finger-tapping test and ANT.

Conclusions: We found limited evidence to support an association between PM_2.5 exposure and fine motor function, attentional function, or working memory in school-aged children.