A data-driven semi-parametric model of SARS-CoV-2 transmission in the United States.

To support decision-making and policy for managing epidemics of emerging pathogens, we present a model for inference and scenario analysis of SARS-CoV-2 transmission in the USA. The stochastic SEIR-type model includes compartments for latent, asymptomatic, detected and undetected symptomatic individuals, and hospitalized cases, and features realistic interval distributions for presymptomatic and symptomatic periods, time varying rates of case detection, diagnosis, and mortality. The model accounts for the effects on transmission of human mobility using anonymized mobility data collected from cellular devices, and of difficult to quantify environmental and behavioral factors using a latent process. The baseline transmission rate is the product of a human mobility metric obtained from data and this fitted latent process. We fit the model to incident case and death reports for each state in the USA and Washington D.C., using likelihood Maximization by Iterated particle Filtering (MIF). Observations (daily case and death reports) are modeled as arising from a negative binomial reporting process. We estimate time-varying transmission rate, parameters of a sigmoidal time-varying fraction of hospitalized cases that result in death, extra-demographic process noise, two dispersion parameters of the observation process, and the initial sizes of the latent, asymptomatic, and symptomatic classes. In a retrospective analysis covering March-December 2020, we show how mobility and transmission strength became decoupled across two distinct phases of the pandemic. The decoupling demonstrates the need for flexible, semi-parametric approaches for modeling infectious disease dynamics in real-time.

Exposure to air pollution during the first 1000 days of life and subsequent health service and medication usage in children.

BACKGROUND: Evidence of health effects following early life exposure to short-to-medium duration of high pollution levels is extremely limited. OBJECTIVES: We aimed to evaluate the associations between: 1. intrauterine exposure to fine particulate matter (PM2.5) from coal mine fire emissions and the frequencies of general practitioner attendances and dispensations of prescribed asthma inhalers, steroid skin creams, and antibiotics during the first year of life; 2. infant exposure and those outcomes during the year following the fire. METHODS: All participants were recruited from the Latrobe Valley of Victoria, Australia. Participants' 24-h average and hourly peak mine fire-specific PM2.5 exposures from 09/02/2014 to 31/03/2014 were estimated using chemical transport modelling. Outcome data were obtained from the Australian Medicare Benefits Schedule and Pharmaceutical Benefits Scheme from each child's birth to 31/12/2016. We used negative binomial and logistic regression models to independently assess risks of the outcomes associated with every 10 and 100 µg m-3 increase in average or peak PM2.5 exposure, respectively, while adjusting for potential confounders. RESULTS: We included 286 of 311 children whose parents consented to be linked, comprising 77 with no exposure, 88 with intrauterine exposure and 121 with exposure in infancy. 10- and 100- µg m-3 increases in average and peak PM2.5 exposure during infancy were associated with greater incidence of antibiotics being dispensed during the year following the fire: the adjusted incidence rate ratios were 1.24 (95% CI 1.02, 1.50, p = 0.036) and 1.14 (1.00, 1.31, p = 0.048) respectively. No other significant associations were observed. CONCLUSION: Exposure to coal mine fire emissions during infancy was associated with increased dispensing of antibiotics. This could reflect increased childhood infections or increased prescriptions of antibiotics in the year following the fire.

Early life exposure to coal mine fire and tobacco smoke affect subclinical vascular function.

OBJECTIVE: To evaluate whether vascular health in young children was associated with exposure to a 6-week episode of coal mine fire smoke or environmental tobacco smoke (ETS) in a retrospective cohort study. METHODS: Three years after a coal mine fire in Victoria, Australia, we investigated the vascular health of children either in utero (n=75) or aged <2 years (postnatal exposure, n=96) at the time of the fire. The outcomes were the carotid intima-media thickness (IMT) and pulse wave velocity (PWV). The mean and peak daily particulate matter <2.5 µm in diameter (PM2.5) exposures were estimated based on their daily locations throughout the fire period. Multivariable linear regression models were used to test for associations between the fire-related PM2.5 and outcomes adjusted for relevant covariates including ETS. RESULTS: In the postnatal-exposure group, each 10 µg/m³ increase in mean PM2.5 level was independently positively associated with PWV (ß=0.116, p=0.028). When these two groups were combined, there was an association between mean PM2.5 and increased PWV in those children who had ETS exposure (ß=0.148, p=0.033) or whose mothers smoked (ß=0.151, p=0.011), but not in those not exposed to ETS or maternal smoking. CONCLUSIONS: Three years after a coal mine fire, infants aged up to 2 years at the time of exposure have increases in vascular stiffness. Although no adverse effects were observed in the in uterus exposure group, further follow-up study is needed to elucidate the long-term effects of coal mine fire smoke exposure.

Early life exposure to coal mine fire smoke emissions and altered lung function in young children.

BACKGROUND AND OBJECTIVE: Long-term respiratory risks following exposure to relatively short periods of poor air quality early in life are unknown. We aimed to evaluate the association between exposure to a 6-week episode of air pollution from a coal mine fire in children aged <2 years, and their lung function 3 years after the fire. METHODS: We conducted a prospective cohort study. Individual exposure to 24-h average and peak concentrations of particulate matter with an aerodynamic diameter <2.5 µm in diameter (PM2.5 ) during the fire were estimated using dispersion and chemical transport modelling. Lung function was measured using the forced oscillation technique (FOT), generating standardized Z-scores for resistance and reactance at a frequency of 5 Hz (Rrs5 and Xrs5 ), and area under the reactance curve (AX). We used linear regression models to assess the associations between PM2.5 exposure and lung function, adjusted for potential confounders. RESULTS: Of the 203 infants originally recruited, 84 aged 4.3 ± 0.5 years completed FOT testing. Median (interquartile range, IQR) for average and peak PM2.5 were 7.9 (6.8-16.8) and 103.4 (60.6-150.7) µg/m3 , respectively. The mean ± SD Z-scores for Rrs5 , Xrs5 and AX were 0.56 ± 0.80, -0.76 ± 0.88 and 0.72 ± 0.92, respectively. After adjustment for potential confounders including maternal smoking during pregnancy, a 10 µg/m3 increase in average PM2.5 was significantly associated with worsening AX (ß-coefficient: 0.260; 95% CI: 0.019, 0.502), while the association between a 100-µg/m3 increase in peak PM2.5 and AX was borderline (0.166; 95% CI: -0.002, 0.334). CONCLUSION: Infant exposure to coal mine fire emissions could be associated with long-term impairment of lung reactance.