ABSTRACT
Objectives. To describe trends in the number of air travelers categorized as infectious with SARS-CoV-2 (severe acute respiratory syndrome coronavirus 2; the virus that causes COVID-19) in the context of total US COVID-19 vaccinations administered, and overall case counts of SARS-CoV-2 in the United States. Methods. We searched the Quarantine Activity Reporting System (QARS) database for travelers with inbound international or domestic air travel, a positive SARS-CoV-2 lab result, and a surveillance categorization of SARS-CoV-2 infection reported during January 2020 to December 2021. Travelers were categorized as infectious during travel if they had arrival dates from 2 days before to 10 days after symptom onset or a positive viral test. Results. We identified 80 715 persons meeting our inclusion criteria; 67 445 persons (83.6%) had at least 1 symptom reported. Of 67 445 symptomatic passengers, 43 884 (65.1%) reported an initial symptom onset date after their flight arrival date. The number of infectious travelers mirrored the overall number of US SARS-CoV-2 cases. Conclusions. Most travelers in the study were asymptomatic during travel, and therefore unknowingly traveled while infectious. During periods of high community transmission, it is important for travelers to stay up to date with COVID-19 vaccinations and consider wearing a high-quality mask to decrease the risk of transmission. (Am J Public Health. 2023;113(8):904-908. https://doi.org/10.2105/AJPH.2023.307325).
Subject(s)
COVID-19 , Communicable Diseases , Humans , United States/epidemiology , SARS-CoV-2 , COVID-19/epidemiology , COVID-19/prevention & control , Travel , QuarantineABSTRACT
Monkeypox is a rare, sometimes life-threatening zoonotic infection that occurs in west and central Africa. It is caused by Monkeypox virus, an orthopoxvirus similar to Variola virus (the causative agent of smallpox) and Vaccinia virus (the live virus component of orthopoxvirus vaccines) and can spread to humans. After 39 years without detection of human disease in Nigeria, an outbreak involving 118 confirmed cases was identified during 2017-2018 (1); sporadic cases continue to occur. During September 2018-May 2021, six unrelated persons traveling from Nigeria received diagnoses of monkeypox in non-African countries: four in the United Kingdom and one each in Israel and Singapore. In July 2021, a man who traveled from Lagos, Nigeria, to Dallas, Texas, became the seventh traveler to a non-African country with diagnosed monkeypox. Among 194 monitored contacts, 144 (74%) were flight contacts. The patient received tecovirimat, an antiviral for treatment of orthopoxvirus infections, and his home required large-scale decontamination. Whole genome sequencing showed that the virus was consistent with a strain of Monkeypox virus known to circulate in Nigeria, but the specific source of the patient's infection was not identified. No epidemiologically linked cases were reported in Nigeria; no contact received postexposure prophylaxis (PEP) with the orthopoxvirus vaccine ACAM2000.
Subject(s)
Mpox (monkeypox) , Humans , Male , Mpox (monkeypox)/diagnosis , Mpox (monkeypox)/epidemiology , Mpox (monkeypox)/prevention & control , Monkeypox virus/genetics , Nigeria/epidemiology , Texas/epidemiologyABSTRACT
Epidemiological studies suggest a link between pesticide exposure and an increased risk of developing Parkinson's disease (PD). Although studies have been unable to clearly identify specific pesticides that contribute to PD, a few human studies have reported higher levels of the organochlorine pesticides dieldrin and DDE (a metabolite of DDT) in post-mortem PD brains. Previously, we found that exposure of mice to dieldrin caused perturbations in the nigrostriatal dopamine system consistent with those seen in PD. Given the concern over the environmental persistence and reintroduction of DDT for the control of malaria-carrying mosquitoes and other pests, we sought to determine whether DDT and its two major metabolites, DDD and DDE, could damage the dopamine system. In vitro analyses in mouse synaptosomes and vesicles demonstrated that DDT and its metabolites inhibit the plasma membrane dopamine transporter (DAT) and the vesicular monoamine transporter (VMAT2). However, exposure of mice to either DDT or DDE failed to show evidence of nigrostriatal damage or behavioral abnormalities in any of the measures examined. Thus, we report that in vitro effects of DDT and its metabolites on components of the dopamine system do not translate into neurotoxicological outcomes in orally exposed mice and DDT appears to have less dopamine toxicity when compared to dieldrin. These data suggest elevated DDE levels in PD patients may represent a measure of general pesticide exposure and that other pesticides may be responsible for the association between pesticide exposure and PD.
Subject(s)
DDT/metabolism , DDT/pharmacology , Dopamine Plasma Membrane Transport Proteins/drug effects , Dopamine Plasma Membrane Transport Proteins/metabolism , Pesticides/pharmacology , Animals , Behavior, Animal/drug effects , Cell Line, Tumor , Chromatography, High Pressure Liquid/methods , Dopamine/metabolism , Dose-Response Relationship, Drug , Fluoresceins/metabolism , Humans , Male , Mice , Mice, Inbred C57BL , Motor Activity/drug effects , Neuroblastoma , Protein Carbonylation/drug effects , Tritium/metabolismABSTRACT
Epidemiological and laboratory studies have suggested that exposure to polychlorinated biphenyls (PCBs) may be a risk factor for Parkinson's disease. The purpose of this study was to examine the potential mechanisms by which PCBs may disrupt normal functioning of the nigrostriatal dopamine (DA) system. We utilized an environmentally relevant exposure of PCBs (7.5 or 15 mg/kg/day Aroclor 1,254:1,260 for 30 days by oral gavage) to identify early signs of damage to the DA system. This dosing regimen, which resulted in PCB levels similar to those found in human brain samples, did not cause overt degeneration to the DA system as shown by a lack of change in striatal DA levels or tyrosine hydroxylase levels. However, we did observe a dramatic dose-dependent decrease in striatal dopamine transporter (DAT) levels. The observed reductions appear to be specific to the DAT populations located in the striatum, as no change was observed in other dopaminergic brain regions or to other neurotransmitter transporters present in the striatum. These data demonstrate that PCB tissue concentrations similar to those found in postmortem human brain specifically disrupt DA transport, which acts as a precursor to subsequent damage to the DA system. Furthermore, DAT imaging may be useful in evaluating alterations in brain function in human populations exposed to PCBs.