Cold weather exposure increases susceptibility to viral respiratory illnesses
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Peer-reviewed scientific literature demonstrates that cold exposure directly impairs nasal antiviral immunity by reducing extracellular vesicle secretion and antiviral binding efficacy, supporting the claim that cold weather increases susceptibility to viral respiratory illnesses.
Background: The human upper respiratory tract is the first site of contact for inhaled respiratory viruses and elaborates an array of innate immune responses. Seasonal variation in respiratory viral infections and the importance of ambient temperature in modulating immune responses to infections have been well recognized; however, the underlying biological mechanisms remain understudied. Objective: We investigated the role of nasal epithelium-derived extracellular vesicles (EVs) in innate Toll-like receptor 3 (TLR3)-dependent antiviral immunity. Methods: We evaluated the secretion and composition of nasal epithelial EVs after TLR3 stimulation in human autologous cells and fresh human nasal mucosal surgical specimens. We also explored the antiviral activity and mechanisms of TLR3-stimulated EVs against respiratory viruses as well as the effect of cool ambient temperature on TLR3-dependent antiviral immunity. Results: We found that polyinosinic:polycytidylic acid, aka poly(I:C), exposure induced a swarm-like increase in the secretion of nasal epithelial EVs via the TLR3 signaling. EVs participated in TLR3-dependent antiviral immunity, protecting the host from viral infections through both EV-mediated functional delivery of miR-17 and direct virion neutralization after binding to virus ligands via surface receptors, including LDLR and ICAM-1. These potent antiviral immune defense functions mediated by TLR3-stimulated EVs were impaired by cold exposure via a decrease in total EV secretion as well as diminished microRNA packaging and antiviral binding affinity of individual EV. Conclusion: TLR3-dependent nasal epithelial EVs exhibit multiple innate antiviral mechanisms to suppress respiratory viral infections. Furthermore, our study provides a direct quantitative mechanistic explanation for seasonal variation in upper respiratory tract infection prevalence.
The common cold is a unique human disease, as it is arguably the most common disease and because of the large number of respiratory viruses causing colds it is one of the most complex of human diseases. This review discusses the respiratory viruses and notes that all these viruses may cause the illness complex recognised as the common cold. The common cold is discussed as part of the “iceberg concept” of disease which ranges from asymptomatic infection to severe illness and death. The factors influencing the incidence of colds are discussed: crowding and sociability, stress, smoking and alcohol, immune status, sex, age, sleep, season, chilling, nutrition and exercise. The mechanism of symptoms related to the innate immune response is explained and symptomatic treatments are tabulated. Morbidity associated with common cold is discussed and possible vaccines.
Background Acute respiratory illnesses, collectively referred to as the "common cold," represent one of the most prevalent conditions worldwide, affecting billions of individuals annually and imposing an enormous socioeconomic burden estimated at over $40 billion per year in the United States alone. Despite their ubiquity, the etiopathogenesis of these conditions remains insufficiently understood and scientifically contested. Contemporary medicine attributes all common cold episodes exclusively to viral infections — predominantly rhinoviruses (30–50%), coronaviruses (10–15%), and other respiratory viruses. However, this monocausal viral paradigm fails to explain several well-documented clinical and epidemiological inconsistencies: the onset of symptoms within minutes of cold exposure (far preceding any possible viral incubation period), the reversibility of symptoms upon rewarming, the absence of fever in a substantial proportion of cases, and the paradoxical age-related pattern of incidence in which elderly individuals — despite progressive immunosenescence — suffer fewer episodes than children or young adults. These unresolved contradictions call for a fundamental reassessment of the pathogenesis of cold-associated respiratory disease. Objective This narrative review critically examines the role of cold exposure and cold stress in the pathogenesis of acute upper respiratory tract disorders and proposes a novel conceptual framework — Acute Cold Respiratory Syndrome (ACRS) —
Cold-related mortality and morbidity remains an important public health problem in the UK and elsewhere. Health burdens have often reported to be higher in the UK compared to other countries with colder climates, however such assessments are usually based on comparison of excess winter mortality indices, which are subject to biases. Daily time-series regression or case-crossover studies provide the best evidence of the acute effects of cold exposure. Such studies report a 6% increase in all-cause deaths in England & Wales for every 1 °C fall in daily mean temperature within the top 5% of the coldest days. In major Scottish cities, a 1 °C reduction in mean temperature below 11 °C was associated with an increase in mortality of 2.9%, 3.4%, 4.8% and 1.7% from all-causes, cardiovascular, respiratory, and non-cardio-respiratory causes respectively. In Northern Ireland, a 1 °C fall during winter months led to increases of 4.5%, 3.9% and 11.2% for all-cause, cardiovascular and respiratory deaths respectively among adults. Raised risks are also observed with morbidity outcomes. Hip fractures among the elderly are only weakly associated with snow and ice conditions in the UK, with the majority of cases occurring indoors. A person's susceptibility to cold weather is affected by both individual- and contextual-level risk factors. Variations in the distributions of health, demographic, socio-economic and built-environment characteristics are likely to explain most differences in cold ris
Chronic Obstructive Pulmonary Disease (COPD) affects 12-16 million people in the United States and is the third-leading cause of death. In developed countries, smoking is the greatest risk factor for the development of COPD, but other exposures also contribute to the development and progression of the disease. Several studies suggest, though are not definitive, that outdoor air pollution exposure is linked to the prevalence and incidence of COPD. Among individuals with COPD, outdoor air pollutants are associated with loss of lung function and increased respiratory symptoms. In addition, outdoor air pollutants are also associated with COPD exacerbations and mortality. There is much less evidence for the impact of indoor air on COPD, especially in developed countries in residences without biomass exposure. The limited existing data suggests that indoor particulate matter and nitrogen dioxide concentrations are linked to increased respiratory symptoms among patients with COPD. In addition, with the projected increases in temperature and extreme weather events in the context of climate change there has been increased attention to the effects of heat exposure. Extremes of temperature-both heat and cold-have been associated with increased respiratory morbidity in COPD. Some studies also suggest that temperature may modify the effect of pollution exposure and though results are not conclusive, understanding factors that may modify susceptibility to air pollution in patients with COP
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