Environmental Epidemiology最新文献

More than half of adolescent children do not get the recommended 8 hours of sleep necessary for optimal growth and development. In adults, several studies have evaluated effects of urban stressors including lack of greenspace, air pollution, noise, nighttime light, and psychosocial stress on sleep duration. Little is known about these effects in adolescents, however, it is known that these exposures vary by socioeconomic status (SES). We evaluated the association between several environmental exposures and sleep in adolescent children in Southern California.

Methods: In 2010, a total of 1476 Southern California Children's Health Study (CHS) participants in grades 9 and 10 (mean age, 13.4 years; SD, 0.6) completed a questionnaire including topics on sleep and psychosocial stress. Exposures to greenspace, artificial light at night (ALAN), nighttime noise, and air pollution were estimated at each child's residential address, and SES was characterized by maternal education. Odds ratios and 95% confidence intervals (95% CIs) for sleep outcomes were estimated by environmental exposure, adjusting for age, sex, race/ethnicity, home secondhand smoke, and SES.

Results: An interquartile range (IQR) increase in greenspace decreased the odds of not sleeping at least 8 hours (odds ratio [OR], 0.86 [95% CI, 0.71, 1.05]). This association was significantly protective in low SES participants (OR, 0.77 [95% CI, 0.60, 0.98]) but not for those with high SES (OR, 1.16 [95%CI, 0.80, 1.70]), interaction P = 0.03. Stress mediated 18.4% of the association among low SES participants.

Conclusions: Residing in urban neighborhoods of greater greenness was associated with improved sleep duration among children of low SES but not higher SES. These findings support the importance of widely reported disparities in exposure and access to greenspace in socioeconomically disadvantaged populations.

Many Chilean cities suffer from high air pollution from industrial, mobile, and residential wood-burning sources. Several studies have linked PM_2.5 air pollution exposure to higher mortality risk from cardiovascular, pulmonary, and lung cancer causes. In recent years, Chile has developed an extensive air pollution monitoring network to enforce air quality standards for PM_2.5, allowing the study of the medium-term association between PM_2.5 and mortality.

Methods: A negative binomial regression model was used to study the association between 3-year average PM_2.5 concentrations and age-adjusted mortality rates for 105 of the 345 municipalities in Chile. Models were fitted for all (ICD10 A to Q codes), cardiopulmonary (I and J), cardiovascular (I), pulmonary (J), cancer (C), and lung cancer (C33-C34) causes; controlling for meteorological, socioeconomic, and demographic characteristics.

Results: A significant association of PM_2.5 exposure with cardiopulmonary (relative risk for 10 µg/m³ PM_2.5: 1.06; 95% confidence interval = 1.00, 1.13) and pulmonary (1.11; 1.02, 1.20) age-adjusted mortality rates was found. Cardiovascular (1.06; 0.99, 1.13) and all causes (1.02; 0.98, 1.07) were positive, but not significant. No significant association was found between cancer and lung cancer. The positive associations remained even when controlling for multiple confounding factors, model specifications, and when considering different methods for exposure characterization. These estimates are in line with results from cohort studies from the United States and European studies.

Conclusion: Three-year average PM_2.5 exposure is positively associated with the age-adjusted mortality rate for cardiopulmonary and cardiovascular causes in Chile. This provides evidence of the medium-term exposure effect of fine particles on long-term mortality rates.

Daily air pollution levels are known to influence the number of patients with acute asthma. We investigated the short-term effects of air pollution exposure on the daily number of asthma medication purchases in the Greater Stockholm area, Sweden.

Methods: We conducted a time-series study with data on asthma medication purchases and daily mean values of particulate matter ≤10 µm (PM₁₀), nitrogen oxides (NO_x), and ozone during 2018-2019. We used nonlinear distributed lag quasi-Poisson regression models to estimate the associations between air pollution levels and medication purchases, adjusting for meteorological variables, pollen levels, day of the week, and long-term trends. The models established linear relationships between air pollutants and the outcome, and potential delayed effects were smoothed with a spline across a lag period of 2 weeks. We applied separate models for each municipality (n = 21) in Greater Stockholm, and calculated pooled estimates to achieve combined results for the whole region.

Results: We observed associations between daily levels of air pollution and purchases of asthma medications, most clearly for PM₁₀. The pooled estimates of the relative risks for asthma medication purchases across all 21 municipalities associated with a 10 μg m^-3 increase in PM₁₀ the same day (lag 0) was 1.7% [95% confidence interval (CI): 1.2%, 2.1%], a cumulative increase of 4.6% (95% CI: 3.7%, 5.6%) over one week (lag 0-6), and a 6.5% (95% CI: 5%, 8%) increase over 2 weeks (lag 0-13). The corresponding pooled effect per 10 μg m^-3 increase in NO_x and ozone were 2.8% (95% CI: 1.6%, 4.1%) and 0.7% (95% CI: 0%, 1.4%) over 2 weeks (lag 0-13), respectively.

Conclusions: Our study revealed short-term associations between air pollution, especially PM₁₀, and purchases of asthma medications.

Exposure to particulate matter with an aerodynamic diameter less than or equal to 2.5 μm (PM_2.5) is associated with increased risk of heart disease, but less is known about the relationship at low concentrations. This study aimed to determine the dose-response relationship between long-term PM_2.5 exposure and risk of incident ischemic heart disease (IHD), incident heart failure (HF), and incident atrial fibrillation (AF) in older men living in a region with relatively low ambient air pollution.

Methods: PM_2.5 exposure was estimated for 11,249 older adult males who resided in Perth, Western Australia and were recruited from 1996 to 1999. Participants were followed until 2018 for the HF and AF outcomes, and until 2017 for IHD. Cox-proportional hazards models, using age as the analysis time, and adjusting for demographic and lifestyle factors were used. PM_2.5 was entered as a restricted cubic spline to model nonlinearity.

Results: We observed a mean PM_2.5 concentration of 4.95 μg/m³ (SD 1.68 μg/m³) in the first year of recruitment. After excluding participants with preexisting disease and adjusting for demographic and lifestyle factors, PM_2.5 exposure was associated with a trend toward increased incidence of IHD, HF, and AF, but none were statistically significant. At a PM_2.5 concentration of 7 μg/m³ the hazard ratio for incident IHD was 1.04 (95% confidence interval [CI] = 0.86, 1.25) compared with the reference category of 1 μg/m³.

Conclusions: We did not observe a significant association between long-term exposure to low-concentration PM_2.5 air pollution and IHD, HF, or AF.

Myocardial infarction (MI) is a leading cause of morbidity and mortality in the United States and its risk increases with extreme temperatures. Climate change causes variability in weather patterns, including extreme temperature events that disproportionately affect socioeconomically disadvantaged communities. Many studies on the health effects of extreme temperatures have considered community-level socioeconomic disadvantage.

Objectives: To evaluate effect modification of the relationship between short-term ambient temperature and MI, by individual-level insurance status (insured vs. uninsured).

Methods: We identified MI hospitalizations and insurance status across New York State (NYS) hospitals from 1995 to 2015 in the New York Department of Health Statewide Planning and Research Cooperative System database, using International Classification of Diseases codes. We linked short-term ambient temperature (averaging the 6 hours preceding the event [MI hospitalization]) or nonevent control period in patient residential zip codes. We employed a time-stratified case-crossover study design for both insured and uninsured strata, and then compared the group-specific rate ratios.

Results: Over the study period, there were 1,095,051 primary MI admissions, 966,475 (88%) among insured patients. During extremely cold temperatures (<5.8 °C) insured patients experienced reduced rates of MI; this was not observed among the uninsured counterparts. At warmer temperatures starting at the 65th percentile (15.7 °C), uninsured patients had higher rates than insured patients (e.g., for a 6-hour pre-event average temperature increase from the median to the 75th percentile, the rate of MI increased was 2.0% [0.0%-4.0%] higher in uninsured group).

Conclusions: Uninsured individuals may face disproportionate rates of MI hospitalization during extreme temperatures.

Outdoor air temperature is associated with increased morbidity and mortality. Other thermal indices theoretically confer greater physiological relevance by incorporating additional meteorological variables. However, the optimal metric for predicting excess deaths or hospitalizations owing to extreme heat among US Medicare beneficiaries remains unknown.

Methods: We calculated daily maximum, minimum, and mean outdoor air temperature (T), heat index (HI), wet-bulb globe temperature (WBGT), and Universal Thermal Climate Index (UTCI) for populous US counties and linked estimates with daily all-cause mortality and heat-related hospitalizations among Medicare beneficiaries (2006-2016). We fit distributed-lag nonlinear models for each metric and compared relative risks (RRs) at the 99th percentile.

Results: Across all heat metrics, extreme heat was statistically significantly associated with elevated risks of morbidity and mortality. Associations were more pronounced for maximum daily values versus the corresponding minimum for the same metric. The starkest example was between HI_max (RR = 1.14; 95% confidence interval [CI] = 1.12, 1.15) and HI_min (RR = 1.10; 95% CI = 1.09, 1.11) for hospitalizations. When comparing RRs across heat metrics, we found no statistically significant differences within the minimum and maximum heat values (i.e., no significant differences between T_max/HI_max/WBGT_max/UTCI_max or between T_min/HI_min/WBGT_min/UTCI_min). We found similar relationships across the National Climate Assessment regions.

Conclusion: Among Medicare beneficiaries in populous US counties, daily maximum and mean values of outdoor heat are associated with greater RRs of heat-related morbidity and all-cause mortality versus minimum values of the same metric. The choice of heat metric (e.g., temperature versus HI) does not appear to substantively affect risk calculations in this population.

Health effects of oxidant gases may be enhanced by components of particulate air pollution that contribute to oxidative stress. Our aim was to examine if within-city spatial variations in the oxidative potential of outdoor fine particulate air pollution (PM_2.5) modify relationships between oxidant gases and cardiovascular mortality.

Methods: We conducted a retrospective cohort study of participants in the Canadian Census Health and Environment Cohort who lived in Toronto or Montreal, Canada, from 2002 to 2015. Cox proportional hazards models were used to estimate associations between outdoor concentrations of oxidant gases (O_x, a redox-weighted average of nitrogen dioxide and ozone) and cardiovascular deaths. Analyses were performed across strata of two measures of PM_2.5 oxidative potential and reactive oxygen species concentrations (ROS) adjusting for relevant confounding factors.

Results: PM_2.5 mass concentration showed little within-city variability, but PM_2.5 oxidative potential and ROS were more variable. Spatial variations in outdoor O_x were associated with an increased risk of cardiovascular mortality [HR per 5 ppb = 1.028, 95% confidence interval (CI): 1.001, 1.055]. The effect of O_x on cardiovascular mortality was stronger above the median of each measure of PM_2.5 oxidative potential and ROS (e.g., above the median of glutathione-based oxidative potential: HR = 1.045, 95% CI: 1.009, 1.081; below median: HR = 1.000, 95% CI: 0.960, 1.043).

Conclusion: Within-city spatial variations in PM_2.5 oxidative potential may modify long-term cardiovascular health impacts of O_x. Regions with elevated O_x and PM_2.5 oxidative potential may be priority areas for interventions to decrease the population health impacts of outdoor air pollution.

There is limited research examining aircraft noise and cardiovascular disease (CVD) risk. The objective of this study was to investigate associations of aircraft noise with CVD among two US cohorts, the Nurses' Health Study (NHS) and Nurses' Health Study II (NHSII).

Methods: Between 1994 and 2014, we followed 57,306 NHS and 60,058 NHSII participants surrounding 90 airports. Aircraft noise was modeled above 44 A-weighted decibels (dB(A)) and linked to geocoded addresses. Based on exposure distributions, we dichotomized exposures at 50 dB(A) and tested sensitivity of this cut-point by analyzing aircraft noise as categories (<45, 45-49, 50-54, ≥55) and continuously. We fit cohort-specific Cox proportional hazards models to estimate relationships between time-varying day-night average sound level (DNL) and CVD incidence and CVD and all-cause mortality, adjusting for fixed and time-varying individual- and area-level covariates. Results were pooled using random effects meta-analysis.

Results: Over 20 years of follow-up, there were 4529 CVD cases and 14,930 deaths. Approximately 7% (n = 317) of CVD cases were exposed to DNL ≥50 dB(A). In pooled analyses comparing ≥50 with <50 dB(A), the adjusted hazard ratio for CVD incidence was 1.00 (95% confidence interval: 0.89, 1.12). The corresponding adjusted hazard ratio for all-cause mortality was 1.02 (95% confidence interval: 0.96, 1.09). Patterns were similar for CVD mortality in NHS yet underpowered.

Conclusions: Among participants in the NHS and NHSII prospective cohorts who generally experience low exposure to aircraft noise, we did not find adverse associations of aircraft noise with CVD incidence, CVD mortality, or all-cause mortality.

Per- and polyfluoroalkyl substances (PFAS) are endocrine-disrupting chemicals that may affect breastfeeding duration. We examined associations between maternal PFAS concentrations during pregnancy and breastfeeding cessation. We investigated potential effect modification by parity status.

Methods: Among 555 women enrolled in the Healthy Start study (2009-2014), we quantified maternal serum concentrations of 5 PFAS during mid- to late-pregnancy (mean 27 weeks of gestation). Participants self-reported their breastfeeding practices through 18-24 months postnatally. Among all participants and stratified by parity, we estimated associations between maternal PFAS concentrations and breastfeeding discontinuation by 3 and 6 months, using Poisson regression, and breastfeeding duration, using Cox regression.

Results: Median PFAS concentrations were similar to those in the general US population. Associations between PFAS and breastfeeding duration differed by parity status. After adjusting for covariates, among primiparous women, associations between PFAS and breastfeeding cessation by 3 and 6 months were generally null, with some inverse associations. Among multiparous women, there were positive associations between perfluorohexane sulfonate, perfluorooctane sulfonate, perfluorooctanoate (PFOA), and perfluorononanoate and breastfeeding cessation by 3 and 6 months. For example, per ln-ng/mL increase in PFOA, the risk ratio for breastfeeding discontinuation by 6 months was 1.45 (95% confidence interval, 1.18, 1.78). Hazard ratios reflected similar patterns between PFAS and breastfeeding duration.

Conclusions: Among primiparous women, we did not find evidence for associations between PFAS concentrations and breastfeeding duration. In contrast, among multiparous women, PFAS serum concentrations were generally inversely associated with breastfeeding duration, though estimates may be biased due to confounding by unmeasured previous breastfeeding.

The frequency and severity of wildfires in the Western United States have increased over recent decades, motivating hypotheses that wildfires contribute to the incidence of coccidioidomycosis, an emerging fungal disease in the Western United States with sharp increases in incidence observed since 2000. While coccidioidomycosis outbreaks have occurred among wildland firefighters clearing brush, it remains unknown whether fires are associated with an increased incidence among the general population.

Methods: We identified 19 wildfires occurring within California's highly endemic San Joaquin Valley between 2003 and 2015. Using geolocated surveillance records, we applied a synthetic control approach to estimate the effect of each wildfire on the incidence of coccidioidomycosis among residents that lived within a hexagonal buffer of 20 km radii surrounding the fire.

Results: We did not detect excess cases due to wildfires in the 12 months (pooled estimated percent change in cases: 2.8%; 95% confidence interval [CI] = -29.0, 85.2), 13-24 months (7.9%; 95% CI = -27.3, 113.9), or 25-36 months (17.4%; 95% CI = -25.1, 157.1) following a wildfire. When examined individually, we detected significant increases in incidence following three of the 19 wildfires, all of which had relatively large adjacent populations, high transmission before the fire, and a burn area exceeding 5,000 acres.

Discussion: We find limited evidence that wildfires drive increases in coccidioidomycosis incidence among the general population. Nevertheless, our results raise concerns that large fires in regions with ongoing local transmission of Coccidioides may be associated with increases in incidence, underscoring the need for field studies examining Coccidioides spp. in soils and air pre- and post-wildfires.