Key Points Question What risk factors and mechanisms can help explain documented allergic reactions to Food and Drug Administration–authorized mRNA COVID-19 vaccines? Findings In this case series of 22 patients with suspected vaccine allergy receiving clinical skin prick testing (SPT) and basophil activation testing (BAT) to the whole vaccine and key components (ie, polyethylene glycol [PEG] and polysorbate 80), none exhibited immunoglobulin (Ig) E–mediated allergy to components via SPT. However, most had positive BAT results to PEG, and all had positive BAT results to their administered mRNA vaccine, with no patient sample having detectable PEG IgE. Meaning These findings suggest that non–IgE-mediated allergic reactions to PEG may be responsible for many documented cases of allergy to mRNA vaccines.
The disease burden associated with air pollution continues to grow. The World Health Organization (WHO) estimates ≈7 million people worldwide die yearly from exposure to polluted air, half of which—3.3 million—are attributable to cardiovascular disease (CVD), greater than from major modifiable CVD risks including smoking, hypertension, hyperlipidemia, and diabetes mellitus. This serious and growing health threat is attributed to increasing urbanization of the world's populations with consequent exposure to polluted air. Especially vulnerable are the elderly, patients with pre‐existing CVD, and children. The cumulative lifetime burden in children is particularly of concern because their rapidly developing cardiopulmonary systems are more susceptible to damage and they spend more time outdoors and therefore inhale more pollutants. World Health Organization estimates that 93% of the world's children aged <15 years—1.8 billion children—breathe air that puts their health and development at risk. Here, we present growing scientific evidence, including from our own group, that chronic exposure to air pollution early in life is directly linked to development of major CVD risks, including obesity, hypertension, and metabolic disorders. In this review, we surveyed the literature for current knowledge of how pollution exposure early in life adversely impacts cardiovascular phenotypes, and lay the foundation for early intervention and other strategies that can help prevent this damage. We also discuss the need for better guidelines and additional research to validate exposure metrics and interventions that will ultimately help healthcare providers reduce the growing burden of CVD from pollution.
Both genes and the environment shape human health and disease. Although IgE-mediated allergic diseases (atopic diseases) have a genetic component and are more prevalent in individuals with a family history of allergic disease, the observed rapid increases in allergic diseases suggest that environmental factors are the predominant driving forces behind these increases rather than genetic alterations. 1,2 Common atopic diseases include atopic dermatitis, food allergy, allergic rhinitis, and allergic asthma. Human diets and lifestyle have undergone major alterations. The exposome, which is the sum total of all the exposures of an individual in a lifetime, has undergone major shifts in the last few decades, affecting human health and disease. A number of environmental factors have been implicated in the increased prevalence of allergic diseases. Predominant among them are increased exposure to pollutants and decreased exposure to microbes and parasitic infections. Air pollution has increased significantly in the last few decades. The hygiene hypothesis suggests that increased hygiene and lack of exposure to microbes and parasitic infections at an early age prevents the necessary stimulus to train the immune system to develop tolerogenic responses. Lifestyle factors,
We present a tool, simplify-defun, that transforms the definition of a given function into a simplified definition of a new function, providing a proof checked by ACL2 that the old and new functions are equivalent. When appropriate it also generates termination and guard proofs for the new function. We explain how the tool is engineered so that these proofs will succeed. Examples illustrate its utility, in particular for program transformation in synthesis and verification.
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