Abstract
BACKGROUND: Satellite-based PM(2.5) predictions are being used to advance exposure science and air-pollution epidemiology in developed countries; including emerging evidence about the impacts of PM(2.5) on acute health outcomes beyond the cardiovascular and respiratory systems, and the potential modifying effects from individual-level factors in these associations. Research on these topics is lacking in Latin America. METHODS: We used a time-stratified case-crossover study design with 1,479,950 non-accidental deaths from Mexico City Metropolitan Area for the period of 2004-2019. Daily 1×1 km PM(2.5) (median=23.4 μg/m(3); IQR=13.6 μg/m(3)) estimates from our satellite-based regional model were employed for exposure assessment at the sub-municipality level. Associations between PM(2.5) with broad-category (organ-system) and cause-specific mortality outcomes were estimated with distributed lag conditional logistic models. We also fit models stratifying by potential individual-level effect modifiers including; age, sex, and individual SES-related characteristics namely: education, health insurance coverage, and job categories. RESULTS: PM(2.5) exposure was associated with higher total non-accidental, cardiovascular, cerebrovascular, respiratory, and digestive mortality. A 10-μg/m(3) PM(2.5) higher cumulative exposure over one week (lag(06)) was associated with higher cause-specific mortality outcomes including hypertensive disease [2.28% (95%CI: 0.26%-4.33%)], acute ischemic heart disease [1.61% (95%CI: 0.59%-2.64%)], other forms of heart disease [2.39% (95%CI: -0.35%-5.20%)], hemorrhagic stroke [3.63% (95%CI: 0.79%-6.55%)], influenza and pneumonia [4.91% (95%CI: 2.84%-7.02%)], chronic respiratory disease [2.49% (95%CI: 0.71%-4.31%)], diseases of the liver [1.85% (95%CI: 0.31%-3.41%)], and renal failure [3.48% (95%CI: 0.79%-6.24%)]. No differences in effect size of associations were observed between SES strata. CONCLUSIONS: Exposure to PM(2.5) was associated with mortality outcomes beyond the cardiovascular and respiratory systems, including specific death-causes from the digestive and genitourinary systems, with no indications of effect modification by individual SES-related characteristics.