Investigating Lagged County-Level Associations Between Agricultural Pesticide Application and Parkinson’s Disease Mortality in the Conterminous United States
2026· American Journal of Student Research· pp. 309-318· 0 citations
TL;DR
The data do not support a robust county-level association between agricultural pesticide application and later PD mortality, and the apparent weak positive gradient is explained by geographic, demographic, and socioeconomic confounding.
Abstract
Pesticide exposure is among the most studied environmental risk factors for Parkinson’s disease (PD),
but most evidence comes from individual-level designs, and national ecological studies rarely account
for confounding or for the long interval between exposure and disease. This study examined whether
county-level agricultural pesticide application from 1998 to 2002 was associated with later countylevel
PD mortality, and whether any association was robust to exposure definition, spatial structure,
multivariable adjustment, and count-based modeling. County agricultural pesticide estimates from the
U.S. Geological Survey EPest series were linked by Federal Information Processing Standard code to
underlying-cause PD mortality (ICD-10 G20) from CDC WONDER for 2003–2007 and 2008–2012. In
unadjusted and population-only models, log pesticide application was weakly and positively associated
with age-adjusted PD mortality in 2008–2012 (r = .096; population-only β = 0.240, p = .002) and null
in 2003–2007. This weak association was robust to normalizing exposure by land area and to removing
high-use counties. However, it did not survive further scrutiny. Exposure and regression residuals
showed strong positive spatial autocorrelation (Moran’s I ≈ 0.47 and ≈ 0.20, p = .001), violating the
independence assumption; adjustment for population density, region, county age structure, median
household income, and racial composition reduced the 2008–2012 coefficient to essentially zero (β =
0.003, p = .97; partial R² ≈ 0.000); and a negative-binomial count model with a population offset showed
no significant association (incidence rate ratio ≈ 1.06, p = .14). The data therefore do not support a robust
county-level association between agricultural pesticide application and later PD mortality. The apparent
weak positive gradient is explained by geographic, demographic, and socioeconomic confounding. The
study is ecological and hypothesis-generating; stronger inference will require longer exposure windows,
incidence data, individual-level exposure, and chemical-specific histories.
Parkinson disease (PD) is an increasing cause of mortality among older adults, but national studies have generally examined mortality trends, forecasts, spatial variation, or environmental associations separately. We integrated these components to characterize U.S. PD mortality and its regional climate correlates.
This ecological time-series study used CDC WONDER mortality data for U.S. adults aged 65 years or older from 1999 to 2024. Joinpoint regression, exponential smoothing state-space forecasting with rolling-origin validation, state-level Moran's I, lagged count models, nonlinear spline analyses, and principal component analysis of regional climate metrics were applied. Nominal and Benjamini-Hochberg-adjusted
P
values were reported.
From 1999 to 2024, PD deaths increased from 14,225 to 39,671, and the age-adjusted mortality rate increased from 41.42 to 71.58 per 100,000 population (average annual percent change, 1.99%; 95% confidence interval [CI], 1.54%-2.45%;
P
< 0.001). The conditional 2035 projection was 91.35 per 100,000 (95% prediction interval, 75.89–110.89). Across 7,502 rolling-origin predictions, mean absolute error was 9.24, root mean squared error was 12.12, mean bias was -6.48, and 95% interval coverage was 51.7%. State-level spatial autocorrelation was not evident in 2024 (Moran's I = 0.022; permutation
P
= 0.326). Primary lag 0–3 temperature estimates did not remain significant after multiplicity correction (adjusted
P
= 0.304), whereas Northeast lag 0–1 mean and apparent temperature estimates remained significant (rate ratios, 0.920 and 0.932 per 10 degrees F; both adjusted
P
= 0.010). No precipitation or sunlight estimate survived correction (minimum adjusted
P
= 0.142 and 0.308, respectively), and 2 of 72 PCA associations remained significant after correction (adjusted
P
= 0.027 and 0.035).
PD mortality increased markedly among older U.S. adults. Forecasts suggested a continued rise but showed limited long-horizon calibration. Climate associations were regional and largely attenuated after multiplicity correction, supporting cautious, hypothesis-generating interpretation.
Exposure to agrichemicals has been linked to an increased risk of congenital anomalies. A previous study in Nebraska observed an association between single waterborne contaminants and birth defects. However, the joint association between pesticide mixture and birth defects has not been evaluated. This study examines the association of 32 commonly applied pesticides and congenital anomalies.We obtained data from the Nebraska Birth Defects Registry from 1995 to 2014. County-level pesticide-active ingredients from the United States Geological Survey, covering 1992 to 2014, were used for 93 Nebraska counties. The associations between 32 pesticides and birth defect subtypes were assessed using the Generalized Weighted Quantile Sum Regression (gWQS) model, adjusting for race, income, employment, and access to care. We observed a statistically significant positive association trend (P-value <0.05) between the 32 pesticides and birth defect subtypes. The strength of this association was slightly higher for craniofacial defects (β1=0.36, Std error 0.07) than for overall defects (β1=0.33, Std error 0.06), renal or genitourinary defects (β1=0.33, Std error 0.05), and cardiac defects (β1=0.32, Std error 0.05).Glyphosate, metsulfuron, quizalofop, triasulfuron, and efsenvalerate largely contributed to the joint association. Our findings suggest different patterns of joint associations for birth defects, providing further evidence of the effects of pesticide mixtures. Future research should prioritize individual-level studies to validate and extend these ecological associations.
Jabeen Taiba, Cheryl L. Beseler, Muhammad Zahid et al.· Environmental Research: Heal...· 0 citations
Background: Parkinson’s Disease (PD) prevention and treatment are complicated because biological processes underlying PD may begin several years before diagnosis. Previous studies suggest that increased exposure to fine particulate matter (PM2.5) and nitrogen dioxide (NO2) air pollution increases PD morbidity. Methods: We analyzed data from 10,366,083 Medicare fee-for-service beneficiaries (age 65+) in the contiguous United States from 2000 to 2016. We defined “hospitalization with PD” as a beneficiary’s first hospitalization claim with diagnosis codes indicating PD. We linked 10-year exposure histories for PM2.5, NO2, and summer ozone (O3). In a discrete-time survival analysis, we fitted distributed lag models and estimated the lagged associations between air pollution and the odds of first hospitalization with PD. Results: Increased PM2.5 and NO2 exposure at least 4 years before hospitalization was associated with increased odds of hospitalization with PD. Accounting for nonlinearities in exposure-response and 10 years of continuous exposure to PM2.5 at the 90th versus the 0.5th percentile (i.e., 11.8 μg/m3 vs. 3.0 μg/m3), the odds ratio for hospitalization with PD was 1.634 (95% CI: 1.489, 1.792). Similarly, for 10 years of continuous exposure to NO2 at the 90th versus the 0.5th percentile (i.e., 31.7 ppb vs. 3.7 ppb), the odds ratio for hospitalization with PD was 1.474 (95% CI: 1.379, 1.575). Evidence of a relationship between O3 exposure and odds for hospitalization with PD was more limited. Conclusions: Air pollution at least 4 years before hospitalization may increase the odds of hospitalization with PD. Reducing air pollution exposure may have long-term effects on PD prevention.
Scott W. Delaney, Lauren Mock, Veronica A. Wang et al.· Environmental Epidemiology· 0 citations
Cardiovascular disease (CVD) is the leading cause of mortality in the United States, yet the role of atmospheric exposures as independent predictors of county-level CVD mortality remains poorly characterized. We integrated satellite-derived atmospheric data alongside socioeconomic, demographic, and livestock predictors across 24,487 county-year observations in the contiguous United States (2012–2019) and applied an XGBoost model with SHAP-based interpretability to identify the leading predictors of county-level CVD mortality (Test R2 = 0.706, RMSE = 29.55 per 100,000 persons). Four of the top ten predictors came from CAMS/ERA5. Ambient formaldehyde exposure frequency ranked second among all 43 predictors, exceeded only by educational attainment and surpassing poverty rate. Wet-bulb temperature ranked third, Leaf Area Index for High Vegetation ranked seventh, and sulphate aerosol mixing ratio ranked eighth. These variables added county-level prediction information beyond socioeconomic covariates. Integrating atmospheric exposure monitoring into county-level CVD surveillance alongside socioeconomic indicators may improve the identification of high-risk geographies.
S. Shrestha, D. Lary, Shisir Ruwali et al.· AI Sensors· 0 citations
Long-term exposure to ambient fine particulate matter (PM2.5) is the leading environmental risk factor for premature mortality worldwide, yet comprehensive province-level evidence quantifying its health burden across Türkiye remains limited. This study investigated the spatial relationship between long-term PM2.5 exposure and all-cause attributable mortality across all 81 Turkish provinces in 2022 using province-level annual mean PM2.5 concentrations and World Health Organisation (WHO) AirQ+ estimates of PM2.5-attributable deaths among adults aged ≥30 years, assuming a counterfactual concentration of 5 µg/m3. The association between PM2.5 exposure and mortality was evaluated using Pearson and Spearman correlation analyses, ordinary least squares (OLS) regression, a log–log elasticity model, and population-weighted regional and exposure-quartile comparisons, while national temporal indicators for 2010–2023 were reported solely as supplementary context for the primary single-year 2022 cross-sectional analysis. The population-weighted annual mean PM2.5 concentration was 27.0 µg/m3, exceeding the WHO Air Quality Guideline by a factor of 5.4, and all 81 provinces exceeded the recommended threshold. The bivariate OLS model accounted for 41% of the between-province variation in attributable mortality rates (OLS slope = 3.23 additional deaths per 100,000 population for each 1 µg/m3 increase in PM2.5; 95% CI: 2.37–4.10; R2 = 0.41; p < 0.001), while the log–log elasticity model indicated that a 1% increase in PM2.5 concentration was associated with a 0.80% increase in the attributable mortality rate (95% CI: 0.65–0.95). The attributable fraction of natural-cause mortality increased progressively from 8.8% in the lowest exposure quartile to 24.6% in the highest. Nationwide, an estimated 68,440 premature deaths, representing 14.2% of all natural-cause deaths among adults aged ≥30 years, were attributable to PM2.5 exposure. These findings quantify a steep, spatially graded PM2.5-attributable mortality burden across Türkiye. As the attributable estimates derive from the WHO AirQ+ concentration–response function, the gradient describes the magnitude and spatial distribution of the modelled burden rather than an independently estimated exposure–response relationship, and on that basis the results support the adoption of WHO-aligned air-quality standards and accelerated decarbonization strategies to reduce the national health burden attributable to ambient air pollution.
Nebile Özmen, V. Duran, Fatma Şencan et al.· Toxics· 0 citations